TGF-β Cancer Research Results

TGF-β, transforming growth factor-beta: Click to Expand ⟱
Source: HalifaxProj(inhibit) CGL-CS TCGA
Type:
Human malignancies frequently exhibit mutations in the TGF-β pathway, and overactivation of this system is linked to tumor growth by promoting angiogenesis and inhibiting the innate and adaptive antitumor immune responses.
Anti-inflammatory cytokine.
In normal tissues, TGF-β plays an essential role in cell cycle regulation, immune function, and tissue remodeling.
- In early carcinogenesis, TGF-β typically acts as a tumor suppressor by inhibiting cell proliferation and inducing apoptosis.

In advanced cancers, cells frequently become resistant to the growth-inhibitory effects of TGF-β.
- TGF-β then switches roles and promotes tumor progression by stimulating epithelial-to-mesenchymal transition (EMT), cell invasion, metastasis, and immune evasion.

Non-canonical (Smad-independent) pathways, such as MAPK, PI3K/Akt, and Rho signaling, also contribute to TGF-β-mediated responses.

Elevated levels of TGF-β have been detected in many advanced-stage cancers, including breast, lung, colorectal, pancreatic, and prostate cancers.
 - The switch from a tumor-suppressive to a tumor-promoting role is often associated with increased TGF-β production and activation in the tumor microenvironment.

High TGF-β expression or signaling activity is frequently correlated with aggressive disease features, resistance to therapy, increased metastasis, and poorer overall survival in many cancer types.
Scientific Papers found: Click to Expand⟱
6462- 1,8-Cin,    Modes of Action of 1,8-Cineol in Infections and Inflammation
- Review, Var, NA - Review, AD, NA
*BioAv↑, become increasingly clear in the recent years that 1,8-Cineol spreads almost everywhere in the human body after its oral administration, from the gut to the blood to the brain.
*BBB↑,
*AntiViral↑, anti-viral effects have been observed to include numerous bacteria and fungi species.
*Bacteria↓,
*AntiFungal↑,
*Inflam↓, central mode of action of 1,8-Cineol is the inhibition of pro-inflammatory cytokine expression
*BioAv↑, 1,8-Cineol was detectable in nasal tissue samples after its oral administration for 14 days, which indicates the systemic distribution of 1,8-Cineol via the gut and the blood stream
*MUC2↓, significantly reduced expression levels of the mucin genes MUC2 and MUC19 in close association with a significantly attenuated activity of transcription factor NF-κB
*MUC19↓,
*NF-kB↓, reduced the expression levels of transcriptional activator nuclear factor (NF)-kB p65 and expression of intercellular adhesion molecule (ICAM)-1 and vascular cell adhesion molecule (VCAM)-1 in lung tissues
*ICAM-1↓,
*VCAM-1↓,
DNAdam↑, colon cancer cells on the potential genotoxicity of 1,8-Cineol revealed a concentration-dependent increase in oxidative DNA damage, whereas it did not affect the cell viability due to DNA repair mechanisms
*lipid-P↓, suppressing the expression of lipid mediators and prostaglandin D2
*PGE2↓,
*IL4↓, decreased expression levels of different inflammatory cytokines such as interleukin (IL)-4, IL-6 and granulocyte macrophage colony stimulating factor (GM-CSF) in bronchial epithelial cells
*IL6↓,
*IL1β↓, 1,8-Cineol-containing leaf extracts significantly suppressed the expression of pro-inflammatory cytokines IL-1β and IL-6 [
*IL6↓,
eff↑, 1,8-Cineol in combination with ellagic acid has been shown to downregulate different cytokines such as transforming growth factor beta-1 (TGF-β1), Fascin-1 (FSCN1), vascular endothelial growth factor (VEGF) and matrix metalloproteinase-9 (MMP-9) in p
TGF-β↓,
fascin↓,
VEGF↓,
MMP9↓,
*MAPK↓, 1,8-Cineol was shown to suppress the activation of the MAPK/ERK
*ERK↓,
JNK↓, decreased activities of transcription factor NFκB and the JNK (c-Jun N-terminal kinase)/AP-1 (activator protein-1) pathway in the human cancer cell lines U373 and HeLa in response to 1,8-Cineol, the active ingredient of the drug Soledum
Wnt↓, 1,8-Cineol acts as an inhibitor of the Wnt/β-catenin pathway in head and neck squamous cell carcinoma (HNSCC).
β-catenin/ZEB1↓,
GSK‐3β↑, decreased inhibition of glycogen synthase kinase 3 (GSK-3) and reduced levels of WNT11
*neuroP↑, 1,8-Cineol has been shown to have neuroprotective activity.
*GSK‐3β↓, decreased activity of GSK-3 in response to 1,8-Cineol could ameliorate advanced glycation end products,
*AGEs↓,
*BBB↑, eucalyptol reveals an opening effect on the blood–brain barrier
*NLRP3↓, controls inflammation by suppressing the NOD-like receptor pyrin domain-containing 3 (NLRP3) activation

5280- 3BP,    Anticancer Efficacy of the Metabolic Blocker 3-Bromopyruvate: Specific Molecular Targeting
- in-vitro, PC, NA
mtDam↑, 3-BromoPyruvate severely damaged mitochondrial integrity which might have severely affected ATP generation in cancer cells.
HK2↓, 3-BP inhibits hexokinase II (HK2) and TGFbeta1 and enhanced active caspase-3 expression in tumor tissues as compared to untreated control.
TGF-β↓,
Casp3↑,
selectivity↑,

2655- AL,    Allicin and Digestive System Cancers: From Chemical Structure to Its Therapeutic Opportunities
- Review, GC, NA
TGF-β↓, Allicin can reduce the expression of TGF-2 and its receptor after entering directly into gastric cancer cell
cycD1/CCND1↓, followed by not only downexpression of cyclinD1, cyclinE, and cyclin-dependent kinase (CDK),
cycE/CCNE↓,
CDK1↓, cyclin-dependent kinase (CDK)
DNAdam↑, but also causing DNA damage and generating ROS
ROS↑,
BAX↑, Allicin increases the levels of Bax (proapoptotic protein), Bcl-2 (antiapoptotic protein), and JNK
JNK↑,
MMP↓, through reduction in outer mitochondrial membrane potential
p38↑, allicin induces p38 mitogen that could induce the protein kinase (MAPK) and then increase the expression of Fas binding to Fas ligand (Fas L) and finally activate death pathway through activation of cyt C and caspase-8.
MAPK↑,
Fas↑,
Cyt‑c↑,
Casp8↑,
PARP↑, allicin makes caspase-dependent apoptosis through elevating PARP, caspase-3 and caspase-9, which are mediated by enhanced discharging of mitochondria cyt C to the cytosol.
Casp3↑,
Casp9↑,
Ca+2↑, allicin induces apoptosis via increasing the amounts of free Ca2+, ER stress.
ER Stress↑,
P21↑, generating ROS to produce p21 and phospho-p53 (Ser15).
CDK2↓, Then p21 suppressed the CDK-4/6/cyclinD complex, P21-PCNA, P21-CDK2, and subsequently reduced cdk1/cyclinB1 complex for G2/M phase cell cycle arrest
CDK6↑,
TumCCA↑,
CDK4↓, Then p21 suppressed the CDK-4/6/cyclinD complex

5356- AL,    Therapeutic role of allicin in gastrointestinal cancers: mechanisms and safety aspects
- Review, GC, NA
Apoptosis↑, induction of apoptosis, inhibition of proliferation, and disruption of cancer cell signaling pathways, including the MAPK, PI3K/AKT, and NF-κB pathways.
TumCP↓,
MAPK↓,
PI3K↓,
Akt↓,
NF-kB↓,
AntiCan↑, Allicin and its other derivatives, such as diallyl disulfide (DADS) and ajoene, have been found to have strong anticancer potential both in vitro and in vivo.
ChemoSen↑, effectiveness of allicin in augmenting conventional chemotherapy and retarding tumor growth proves that allicin is one of the most efficient complementary therapies.
TumCCA↑, In liver cancer, allicin has been shown to mediate cell cycle arrest and apoptosis
Apoptosis↑,
BioAv↑, Allicin (diallyl thiosulfinate) is a compound that is generated when a garlic clove is crushed
selectivity↑, Furthermore, it has no influence on the growth of healthy intestinal cells when it causes stomach cancer cells to undergo apoptosis
TGF-β↓, Allicin can reduce the production of TGF-β2 and its receptor after directly entering gastric cancer cells.
ROS↑, It induces oxidative stress by generating reactive oxygen species (ROS), leading to DNA damage and activation of key apoptotic mediators such as phospho-p53 and p21 [81].
DNAdam↑,
p‑P53↑,
P21↑,
cycD1/CCND1↓, Additionally, cyclin D1, cyclin E, and cyclin-dependent kinases (CDKs) can all be inhibited by allicin.
cycE/CCNE↓,
CDK4↓, suppressing the CDK-4/6/cyclin D complex
CDK6↓,
MMP↓, By lowering the outer mitochondrial membrane potential (MMP), allicin raises levels of nuclear factor kappa B (NF-κB), the proapoptotic protein Bax, while decreasing the antiapoptotic protein Bcl-2, which leads to apoptosis.
NF-kB↑,
BAX↑,
Bcl-2↓,
ER Stress↑, cellular effects of allicin, including its role in inducing ER stress
Casp↑, enhancing caspase activation and apoptosis-inducing factor (AIF)-mediated cell death.
AIF↑,
Fas↑, increasing Fas receptor expression and its binding to Fas ligand (FasL), leading to apoptosis through caspase-8 and cytochrome c activation.
Casp8↑,
Cyt‑c↑,
cl‑PARP↑, leading to poly (ADP-ribose) polymerase (PARP) cleavage and DNA fragmentation.
Ca+2↑, allicin elevates intracellular free Ca2⁺ levels, causing endoplasmic reticulum (ER) stress, which plays a critical role in apoptosis induction
*NRF2↑, by activating the Nrf2 pathway via KLF9, allicin protects against arsenic trioxide-induced liver damage,
*chemoP↑, Additionally, allicin has shown promise in reducing hepatotoxicity caused by tamoxifen (TAM), a commonly used treatment for hormone-dependent breast cancer
*GutMicro↑, Shi et al. [85] found that allicin can ameliorate high-fat diet-induced obesity in mice by altering their gut microbiome.
CycB/CCNB1↑, DATS impaired cell survival in the G2 phase by significantly upregulating cyclins A2 and B1.
H2S↑, DATS can also react with the cellular thiol glutathione to create H2S gas, which can control several other cellular functions [79].
HIF-1↓, allicin treatment (40 µg/ml) for NSCLC lowers the expression of HIF-1 and HIF-2 in hypoxic cells [73]
RadioS↑, Allicin has been shown to increase the sensitivity of X-ray radiation therapy in colorectal cancer, presumably by suppressing the levels of NF-κB, IKKβ mRNA, p-NF-κB, and p-IKKβ protein expression in vitro and in vivo

1124- ALA,    Alpha lipoic acid inhibits proliferation and epithelial mesenchymal transition of thyroid cancer cells
- in-vitro, Thyroid, BCPAP - in-vitro, Thyroid, HTH-83 - in-vitro, Thyroid, CAL-62 - in-vitro, Thyroid, FTC-133 - in-vivo, NA, NA
TumCP↓,
AMPK↑,
mTOR↓,
TumCMig↓,
TumCI↓,
EMT↓,
E-cadherin↑,
β-catenin/ZEB1↓,
Vim↓,
Snail↓,
Twist↓,
TGF-β↓,
p‑SMAD2↓,
TumCG↓, mouse model

1093- And,    Andrographolide attenuates epithelial‐mesenchymal transition induced by TGF‐β1 in alveolar epithelial cells
- in-vitro, Lung, A549
TGF-β↓,
TumCMig↓,
MMP2↓,
MMP9↓,
ECM/TCF↓,
p‑SMAD2↓,
p‑SMAD3↓,
SMAD4↓,
p‑ERK↓,
ROS↓, reduced (TGF‐β1‐induced) intracellular ROS generation
NOX4↓,
SOD2↑,
SIRT1↑, Andro protects AECs from EMT partially by activating Sirt1/FOXO3‐mediated anti‐oxidative stress pathway
FOXO3↑,

307- Api,    Flavonoids inhibit angiogenic cytokine production by human glioma cells
- in-vitro, GBM, GL-15
TGF-β↓,

238- Api,    Apigenin inhibits TGF-β-induced VEGF expression in human prostate carcinoma cells via a Smad2/3- and Src-dependent mechanism
- in-vitro, Pca, PC3 - in-vitro, Pca, LNCaP - in-vitro, Pca, C4-2B
VEGF↓,
TGF-β↓,
Src↓,
FAK↓,
Akt↓,
SMAD2↓,
SMAD3↓,

2318- Api,    Apigenin as a multifaceted antifibrotic agent: Therapeutic potential across organ systems
- Review, Nor, NA
*ROS↓, Apigenin reduces fibrosis by targeting oxidative stress, fibroblast activation, and ECM buildup across organs
*PKM2↓, PKM2-HIF-1α pathway inhibited
*Hif1a↓,
*TGF-β↓, apigenin suppresses the PKM2-HIF-1α and TGF-β signaling pathways to prevent fibrosis
*AMPK↑, In the kidneys, it activates AMPK to suppress TGF-β1-induced fibroblast transformation
*Inflam↓, For the brain, apigenin reduces inflammation and oxidative stress through the PI3K/Akt/Nrf2 pathway.
*PI3K↓, Apigenin exerts neuroprotective effects in neonatal hypoxic-ischemic (HI) brain injury by activating the PI3K/Akt/Nrf2 signaling pathway, which is critical in defending neurons from oxidative stress and inflammation.
*Akt↑,
*NRF2↑, apigenin reduces oxidative damage through Nrf2 and NF-κB pathway modulation
*NF-kB↓, downregulates critical TGF-β and NF-κB pathways.

3383- ART/DHA,    Dihydroartemisinin: A Potential Natural Anticancer Drug
- Review, Var, NA
TumCP↓, DHA exerts anticancer effects through various molecular mechanisms, such as inhibiting proliferation, inducing apoptosis, inhibiting tumor metastasis and angiogenesis, promoting immune function, inducing autophagy and endoplasmic reticulum (ER) stres
Apoptosis↑,
TumMeta↓,
angioG↓,
TumAuto↑,
ER Stress↑,
ROS↑, DHA could increase the level of ROS in cells, thereby exerting a cytotoxic effect in cancer cells
Ca+2↑, activation of Ca2+ and p38 was also observed in DHA-induced apoptosis of PC14 lung cancer cells
p38↑,
HSP70/HSPA5↓, down-regulation of heat-shock protein 70 (HSP70) might participate in the apoptosis of PC3 prostate cancer cells induced by DHA
PPARγ↑, DHA inhibited the growth of colon tumor by inducing apoptosis and increasing the expression of peroxisome proliferator-activated receptor γ (PPARγ)
GLUT1↓, DHA was shown to inhibit the activity of glucose transporter-1 (GLUT1) and glycolytic pathway by inhibiting phosphatidyl-inositol-3-kinase (PI3K)/AKT pathway and downregulating the expression of hypoxia inducible factor-1α (HIF-1α)
Glycolysis↓, Inhibited glycolysis
PI3K↓,
Akt↓,
Hif1a↓,
PKM2↓, DHA could inhibit the expression of PKM2 as well as inhibit lactic acid production and glucose uptake, thereby promoting the apoptosis of esophageal cancer cells
lactateProd↓,
GlucoseCon↓,
EMT↓, regulating the EMT-related genes (Slug, ZEB1, ZEB2 and Twist)
Slug↓, Downregulated Slug, ZEB1, ZEB2 and Twist in mRNA level
Zeb1↓,
ZEB2↓,
Twist↓,
Snail?, downregulated the expression of Snail and PI3K/AKT signaling pathway, thereby inhibiting metastasis
CAFs/TAFs↓, DHA suppressed the activation of cancer-associated fibroblasts (CAFs) and mouse cancer-associated fibroblasts (L-929-CAFs) by inhibiting transforming growth factor-β (TGF-β signaling
TGF-β↓,
p‑STAT3↓, blocking the phosphorylation of STAT3 and polarization of M2 macrophages
M2 MC↓,
uPA↓, DHA could inhibit the growth and migration of breast cancer cells by inhibiting the expression of uPA
HH↓, via inhibiting the hedgehog signaling pathway
AXL↓, DHA acted as an Axl inhibitor in prostate cancer, blocking the expression of Axl through the miR-34a/miR-7/JARID2 pathway, thereby inhibiting the proliferation, migration and invasion of prostate cancer cells.
VEGFR2↓, inhibition of VEGFR2-mediated angiogenesis
JNK↑, JNK pathway activated and Beclin 1 expression upregulated.
Beclin-1↑,
GRP78/BiP↑, Glucose regulatory protein 78 (GRP78, an ER stress-related molecule) was upregulated after DHA treatment.
eff↑, results demonstrated that DHA-induced ER stress required iron
eff↑, DHA was used in combination with PDGFRα inhibitors (sunitinib and sorafenib), it could sensitize ovarian cancer cells to PDGFR inhibitors and achieved effective therapeutic efficacy
eff↑, DHA combined with 2DG (a glycolysis inhibitor) synergistically induced apoptosis through both exogenous and endogenous apoptotic pathways
eff↑, histone deacetylase inhibitors (HDACis) enhanced the anti-tumor effect of DHA by inducing apoptosis.
eff↑, DHA enhanced PDT-induced cell growth inhibition and apoptosis, increased the sensitivity of esophageal cancer cells to PDT by inhibiting the NF-κB/HIF-1α/VEGF pathway
eff↑, DHA was added to magnetic nanoparticles (MNP), and the MNP-DHA has shown an effect in the treatment of intractable breast cancer
IL4↓, downregulated IL-4;
DR5↑, Upregulated DR5 in protein, Increased DR5 promoter activity
Cyt‑c↑, Released cytochrome c from the mitochondria to the cytosol
Fas↑, Upregulated fas, FADD, Bax, cleaved-PARP
FADD↑,
cl‑PARP↑,
cycE/CCNE↓, Downregulated Bcl-2, Bcl-xL, procaspase-3, Cyclin E, CDK2 and CDK4
CDK2↓,
CDK4↓,
Mcl-1↓, Downregulated Mcl-1
Ki-67↓, Downregulated Ki-67 and Bcl-2
Bcl-2↓,
CDK6↓, Downregulated of Cyclin E, CDK2, CDK4 and CDK6
VEGF↓, Downregulated VEGF, COX-2 and MMP-9
COX2↓,
MMP9↓,

556- ART/DHA,    Artemisinins as a novel anti-cancer therapy: Targeting a global cancer pandemic through drug repurposing
- Review, NA, NA
IL6↓,
IL1↓, IL-1β
TNF-α↓,
TGF-β↓, TGF-β1
NF-kB↓,
MIP2↓,
PGE2↓,
NO↓,
Hif1a↓,
KDR/FLK-1↓,
VEGF↓,
MMP2↓,
TIMP2↑,
ITGB1↑,
NCAM↑,
p‑ATM↑,
p‑ATR↑,
p‑CHK1↑,
p‑Chk2↑,
Wnt/(β-catenin)↓,
PI3K↓,
Akt↓,
ERK↓, ERK1/2
cMyc↓,
mTOR↓,
survivin↓,
cMET↓,
EGFR↓,
cycD1/CCND1↓,
cycE1↓,
CDK4/6↓,
p16↑,
p27↑,
Apoptosis↑,
TumAuto↑,
Ferroptosis↑,
oncosis↑,
TumCCA↑, G0/G1 into M phase, G0/G1 into S phase, G1 and G2/M
ROS↑, ovarian cancer cell line model, artesunate induced oxidative stress, DNA double-strand breaks (DSBs) and downregulation of RAD51 foci
DNAdam↑,
RAD51↓,
HR↓,

563- ART/DHA,    Artesunate down-regulates immunosuppression from colorectal cancer Colon26 and RKO cells in vitro by decreasing transforming growth factor β1 and interleukin-10
- in-vitro, Colon, colon26 - in-vitro, CRC, RKO
TGF-β↓,
IL10↓,

1075- ART/DHA,    Artemisinin derivatives inactivate cancer-associated fibroblasts through suppressing TGF-β signaling in breast cancer
- in-vitro, Nor, L929
*TGF-β↓,

1173- Ash,    Withaferin A inhibits proliferation of human endometrial cancer cells via transforming growth factor-β (TGF-β) signalling
- in-vitro, EC, K1 - in-vitro, Nor, THESCs
TumCP↓,
*toxicity↓, comparatively lower toxicity against the THESCs normal cells
Apoptosis↑,
TumCCA↑, G2/M cell cycle arrest
TumCMig↓, 53%
TumCI↓, 40%
p‑SMAD2↓,
TGF-β↓,
*toxicity↓, Cytotoxicity of withaferin A was comparatively lower against normal THESCs endometrial cells (IC50 value of 76 µM) when compared to cancerous KLE cells.

3155- Ash,    Overview of the anticancer activity of withaferin A, an active constituent of the Indian ginseng Withania somnifera
- Review, Var, NA
Half-Life↝, The pharmacokinetic study demonstrates that a dose of 4 mg/kg in mice results in 2 μM concentration in plasma (with a half-life of 1.3 h, in the breast cancer model of mice),
Inflam↓, WA has many biological activities: anti-inflammatory (Dubey et al. 2018), immunomodulatory (Davis and Girija 2000), antistress (Singh et al. 2016), antioxidant (Sumathi et al. 2007) and anti-angiogenesis
antiOx↓,
angioG↓,
ROS↑, WA induces oxidative stress (ROS) determining mitochondrial dysfunction as well as apoptosis in leukaemia cells
BAX↑, withaferin mediates apoptosis by ROS generation and activation of Bax/Bak.
Bak↑,
E6↓, The results of the study show that withaferin treatment downregulates the HPV E6 and E7 oncoprotein and induces accumulation of p53 result in the activation of various apoptotic markers (e.g. Bcl2, Bax, caspase-3 and cleaved PARP).
E7↓,
P53↑,
Casp3↑,
cl‑PARP↑,
STAT3↓, WA treatment also decreases the level of STAT3
eff↑, This study concludes that combination of DOX with WA can reduce the doses and side effects of the treatment which gives valuable possibilities for future research.
HSP90↓, by inhibiting the HSP90
TGF-β↓, WA inhibited TGFβ1 and TNFα- induced EMT;
TNF-α↓,
EMT↑,
mTOR↓, by downregulation of mTOR/STAT3 signalling.
NOTCH1↓, WA showed inhibition of pro-survival signalling markers (Notch1, pAKT and NFκB)
p‑Akt↓,
NF-kB↓,
Dose↝, WA dose escalation sets consisted of 72, 108, 144 and 216 mg, fractioned in 2-4 doses/day.

5502- Ba,    An overview of pharmacological activities of baicalin and its aglycone baicalein: New insights into molecular mechanisms and signaling pathways
- Review, Var, NA
*AntiCan↑, antibacterial, antiviral, anticancer, anticonvulsant, anti-oxidant, hepatoprotective, and neuroprotective effects.
*antiOx↑,
*hepatoP↑,
*neuroP↑,
*ROS↓, pharmacological properties of baicalin and baicalein are due to their abilities to scavenge reactive oxygen species (ROS)
Ca+2↑, Baicalein mainly induced apoptosis through Ca+2 influx via Ca2+ release from the reticulum to cytosol dependent on phospholipase C protein
ROS↑, ROS production is associated with baicalein-induced apoptosis via Ca2+-dependent apoptosis in tongue and breast cancer cells (78, 79)
BAX↑, The level of Bax/Bcl-2 increased and caspase-3 and -9 were activated following the release of cytochrome C (80).
Casp3↑,
Casp9↑,
Cyt‑c↑,
MMP↓, In gastric cancer cells, baicalein mediated apoptosis in a dose-dependent manner through disruption of mitochondrial membrane potential
Mcl-1↓, In pancreatic cancer cells, baicalein induced apoptosis via suppression of the Mcl-1 protein.
PI3K↓, In HepG2 cells, baicalin-copper induced apoptosis through down-regulation of phosphoinositide-3 kinase/protein kinase B/mammalian target of rapamycin (PI3K/Akt/mTOR) signaling pathway
Akt↓,
mTOR↓,
BAD↓, Studies demonstrated that baicalein treatment suppressed Bad, ERK1/2 phosphorylation, and MEK1 expression both in vitro and in vivo.
ERK↓,
MEK↓,
DR5↑, Baicalein enhanced the activity of death receptor-5 (DR5) in prostate cancer PC3 cells.
Fas↑, baicalin is the active ingredient that acts as Fas ligand and caused up-regulation of Fas protein (89).
TumMeta↓, Baicalin/baicalein not only induced apoptosis in cancer cells but also suppressed metastasis.
EMT↓, both baicalin and baicalein inhibited epithelial-mesenchymal transition (EMT) through the suppression of TGF-β in breast epithelial cells through the NF-κB pathway (92).
SMAD4↓, baicalein suppressed metastasis in gastric cancer through inactivation of the Smad4/TGF-β pathway (93).
TGF-β↓,
MMP9↓, baicalin and baicalein inhibition of the expression level of matrix metalloproteinases (MMP) such as MMP-9 and MMP-2 in liver, breast, lung, ovarian, gastric, and colorectal cancers and glioma
MMP2↓,
HIF-1↓, Baicalin attenuated lung metastasis through inhibition of hypoxia-inducible factor (HIF)
12LOX↓, Baicalein acts as an anticancer agent via inhibiting 12-lipooxygenase (12-LOX),

5501- Ba,    Therapeutic effects and mechanisms of action of Baicalein on stomach cancer: a comprehensive systematic literature review
- Review, GC, NA
AntiCan↑, The review demonstrated that BC exerts therapeutic effects on GC through multiple biochemical mechanisms.
Apoptosis↑, BC plays an important role in inducing apoptosis, inhibiting cell proliferation, and suppressing metastasis in GC cells.
TumCP↓,
TumMeta↓,
BAX↑, graphical abstract
TumAuto↑,
ROS↑,
NRF2↝, BC induced apoptosis and autophagy in MGC-803, SGC-7901, and HGC-27 cells, enhancing cisplatin sensitivity via suppression of the AKT/mTOR pathway and modulation of the Nrf2/Keap1 axis.
PI3K↓,
Akt↓,
NF-kB↓,
TGF-β↓,
SMAD4↓,
GPx4↓, It induces autophagy and ferroptosis, partly through p53 activation and suppression of SLC7A11/GPX4, and disrupts mitochondrial membrane potential via reactive oxygen species (ROS) generation [31, 37]
MMP↓,
*HO-1↑, BC stabilizes Nrf2, leading to the induction of antioxidant enzymes such as HO-1, GST, and NQO1, which mitigate oxidative stress and contribute to its antitumor effects [38].
*GSTs↑,
*antiOx↑,
*AntiTum↑,
*NRF2↑,
ChemoSen↑, BC induced apoptosis and autophagy in MGC-803, SGC-7901, and HGC-27 cells, enhancing cisplatin sensitivity via suppression of the AKT/mTOR pathway and modulation of the Nrf2/Keap1 axis.
Akt↓,
mTOR↓,
FAK↓, reducing FAK expression
Ki-67↓, Immunohistochemical analysis also revealed lower Ki-67 levels, indicating reduced cellular proliferation.

2606- Ba,    Baicalein: A review of its anti-cancer effects and mechanisms in Hepatocellular Carcinoma
- Review, HCC, NA
ChemoSen↑, In addition, the combination of baicalein and silymarin eradicates HepG2 cells efficiently superior to baicalein or silymarin alone
TumCP↓, Cell viability assays have demonstrated that baicalein is significantly cytotoxic against several HCC cell lines and can inhibit the proliferation of HCC cells through arresting the cell cycle.
TumCCA↑,
TumCMig↓, Baicalein has been proved to inhibit migration and invasion of human HCC cells by reducing the expression and their proteinase activity of matrix metalloproteinases (MMPs),
TumCI↓,
MMPs↓,
MAPK↓, A large number of studies found that baicalein could inhibit migration and invasion of cancer cells by targeting the MAPK, TGF-b/Smad4, GPR30 pathway and molecules such as, ezrin, zinc-finger protein X-linked (ZFX),
TGF-β↓,
ZFX↓,
p‑MEK↓, Baicalein could inhibited the phosphorylation of MEK1 and ERK1/2, leading to decreased expression and proteinase activity of MMP-2/9 and urokinase-type plasminogen activator (u-PA),
ERK↓,
MMP2↓,
MMP9↓,
uPA↓,
TIMP1↓, as well as increased expression of TIMP-1 and TIMP-2
TIMP2↓,
NF-kB↓, Additionally, the nuclear translocation of NF-kB/p50 and p65/RelA and the phosphorylation of I-kappa-B (IKB)-b could be down-regulated by baicalein
p65↓,
p‑IKKα↓,
Fas↑, Hep3 B cells via activating Fas, Caspase -2, -3, -8, -9, down-regulating Bcl-xL, and upregulating Bax [
Casp2↑,
Casp3↑,
Casp8↑,
Casp9↑,
Bcl-xL↓,
BAX↑,
ER Stress↑, baicalein could induced apoptosis via endoplasmic reticulum (ER) stress in SMMC-7721 and Bel-7402
Ca+2↑, increasing intracellular calcium(Ca2+ ), and activating JNK pathwa
JNK↑,
P53↑, selectively induce apoptosis in HCC J5 cells via upregulation of p53
ROS↑, baicalein could induced cell apoptosis through regulating ROS via increasing intracellular H2O 2 level [
H2O2↑,
cMyc↓, baicalein could promote apoptosis in HepG2 and Bel-7402 cells through inhibiting c-Myc and CD24 expression
CD24↓,
12LOX↓, baicalein could induced cell apoptosis in SMMC-7721 and HepG2 cells by specifically inhibiting expression of 12-lipoxygenase(12-LOX), a critical anti-apoptotic genes

1399- BBR,  Rad,    Radiotherapy Enhancing and Radioprotective Properties of Berberine: A Systematic Review
- Review, NA, NA
*ROS↓, normal cells
*MDA↓, normal cells
*TNF-α↓, normal cells
*TGF-β↓, TGF-β1 normal cells
*IL10↑, normal cells
ROS↑, cancer cells
DNAdam↑, cancer cells
mtDam↑, cancer cells
MMP↓, cancer cells
Apoptosis↑, cancer cells
TumCCA↑, cancer cells
Hif1a↓, cancer cells
VEGF↓, cancer cells
RadioS↑, revealed radiosensitizing properties

2674- BBR,    Berberine: A novel therapeutic strategy for cancer
- Review, Var, NA - Review, IBD, NA
Inflam↓, anti-inflammatory, antidiabetic, antibacterial, antiparasitic, antidiarrheal, antihypertensive, hypolipidemic, and fungicide.
AntiCan↑, elaborated on the anticancer effects of BBR through the regulation of different molecular pathways such as: inducing apoptosis, autophagy, arresting cell cycle, and inhibiting metastasis and invasion.
Apoptosis↑,
TumAuto↑,
TumCCA↑,
TumMeta↓,
TumCI↓,
eff↑, BBR is shown to have beneficial effects on cancer immunotherapy.
eff↑, BBR inhibited the release of Interleukin 1 beta (IL-1β), Interferon gamma (IFN-γ), Interleukin 6 (IL-6), and Tumor Necrosis Factor-alpha (TNF-α) from LPS stimulated lymphocytes by acting as a dopamine receptor antagonist
CD4+↓, BBR inhibited the proliferation of CD4+ T cells and down-regulated TNF-α and IL-1 and thus, improved autoimmune neuropathy.
TNF-α↓,
IL1↓,
BioAv↓, On the other hand, P-Glycoprotein (P-gp), a secretive pump located in the epithelial cell membrane, restricts the oral bioavailability of a variety of medications, such as BBR. The use of P-gp inhibitors is a common and effective way to prevent this
BioAv↓, Regardless of its low bioavailability, BBR has shown great therapeutic efficacy in the treatment of a number of diseases.
other↓, BBR has been also used as an effective therapeutic agent for Inflammatory Bowel Disease (IBD) for several years
AMPK↑, inhibitory effects on inflammation by regulating different mechanisms such as 5′ Adenosine Monophosphate-Activated Protein Kinase (AMPK. Increase of AMPK
MAPK↓, Mitogen-Activated Protein Kinase (MAPK), and NF-κB signaling pathways
NF-kB↓,
IL6↓, inhibiting the expression of proinflammatory genes such as IL-1, IL-6, Monocyte Chemoattractant Protein 1 (MCP1), TNF-α, Prostaglandin E2 (PGE2), and Cyclooxygenase-2 (COX-2)
MCP1↓,
PGE2↓,
COX2↓,
*ROS↓, BBR protected PC-12 cells (normal) from oxidative damage by suppressing ROS through PI3K/AKT/mTOR signaling pathways
*antiOx↑, BBR therapy improved the antioxidant function of mice intestinal tissue by enhancing the levels of glutathione peroxidase and catalase enzymes.
*GPx↑,
*Catalase↑,
AntiTum↑, Besides, BBR leaves great antitumor effects on multiple types of cancer such as breast cancer,69 bladder cancer,70 hepatocarcinoma,71 and colon cancer.72
TumCP↓, BBR exerts its antitumor activity by inhibiting proliferation, inducing apoptosis and autophagy, and suppressing angiogenesis and metastasis
angioG↓,
Fas↑, by increasing the amounts of Fas receptor (death receptor)/FasL (Fas ligand), ROS, ATM, p53, Retinoblastoma protein (Rb), caspase-9,8,3, TNF-α, Bcl2-associated X protein (Bax), BID
FasL↑,
ROS↑,
ATM↑,
P53↑,
RB1↑,
Casp9↑,
Casp8↑,
Casp3↓,
BAX↑,
Bcl-2↓, and declining Bcl2, Bcl-X, c-IAP1 (inhibitor of apoptosis protein), X-linked inhibitor of apoptosis protein (XIAP), and Survivin levels
Bcl-xL↓,
IAP1↓,
XIAP↓,
survivin↓,
MMP2↓, Furthermore, BBR suppressed Matrix Metalloproteinase-2 (MMP-2), and MMP-9 expression.
MMP9↓,
CycB/CCNB1↓, Inhibition of cyclin B1, cdc2, cdc25c
CDC25↓,
CDC25↓,
Cyt‑c↑, BBR inhibited tumor cell proliferation and migration and induced mitochondria-mediated apoptosis pathway in Triple Negative Breast Cancer (TNBC) by: stimulating cytochrome c release from mitochondria to cytosol
MMP↓, decreased the mitochondrial membrane potential, and enabled cytochrome c release from mitochondria to cytosol
RenoP↑, BBR significantly reduced the destructive effects of cisplatin on the kidney by inhibiting autophagy, and exerted nephroprotective effects.
mTOR↓, U87 cell, Inhibition of m-TOR signaling
MDM2↓, Downregulation of MDM2
LC3II↑, Increase of LC3-II and beclin-1
ERK↓, BBR stimulated AMPK signaling, resulting in reduced extracellular signal–regulated kinase (ERK) activity and COX-2 expression in B16F-10 lung melanoma cells
COX2↓,
MMP3↓, reducing MMP-3 in SGC7901 GC and AGS cells
TGF-β↓, BBR suppressed the invasion and migration of prostate cancer PC-3 cells by inhibiting TGF-β-related signaling molecules which induced Epithelial-Mesenchymal Transition (EMT) such as Bone morphogenetic protein 7 (BMP7),
EMT↑,
ROCK1↓, inhibiting metastasis-associated proteins such as ROCK1, FAK, Ras Homolog Family Member A (RhoA), NF-κB and u-PA, leading to in vitro inhibition of MMP-1 and MMP-13.
FAK↓,
RAS↓,
Rho↓,
NF-kB↓,
uPA↓,
MMP1↓,
MMP13↓,
ChemoSen↑, recent studies have indicated that it can be used in combination with chemotherapy agents

2763- BetA,    Betulinic Acid Inhibits the Stemness of Gastric Cancer Cells by Regulating the GRP78-TGF-β1 Signaling Pathway and Macrophage Polarization
- in-vitro, GC, NA
GRP78/BiP↓, The results indicated that BA inhibited not only GRP78-mediated stemness-related protein expression and GRP78-TGF-β-mediated macrophage polarization
TGF-β↓, BA Inhibits the Expression of GRP78, TGF-β1, and Stemness Markers in Human Gastric Cancer Cells
ChemoSen↑, BA is a promising candidate for clinical application in combination-chemotherapy targeting cancer stemness.
CSCs↓,
SMAD2↓, BA inhibited TGF-β/Smad2/3 signaling, TGF-β1 secretion, and OCT4 expression in a dose-dependent manner
SMAD3↓,
OCT4↓,

1206- Caff,    Caffeine inhibits TGFβ activation in epithelial cells, interrupts fibroblast responses to TGFβ, and reduces established fibrosis in ex vivo precision-cut lung slices
- in-vitro, NA, NA - ex-vivo, NA, NA
Fibrosis↓,
TGF-β↓, inhibited TGFβ activation by lung epithelial cells in a concentration-dependent manner but had no effect on TGFβ activation in fibroblasts.
α-SMA↓,

1105- CEL,    Celecoxib inhibits the epithelial-to-mesenchymal transition in bladder cancer via the miRNA-145/TGFBR2/Smad3 axis
- in-vitro, BC, NA
COX2↓, Celecoxib, a selective cyclooxygenase-2 inhibitor
TumCP↓,
TumCMig↓,
TumCI↓,
EMT↓,
miR-145↑,
TGF-β↓,
SMAD3↓,

1601- Cu,    The copper (II) complex of salicylate phenanthroline induces immunogenic cell death of colorectal cancer cells through inducing endoplasmic reticulum stress
- in-vitro, CRC, NA
i-CRT↓, Cu(sal)phen induced the release of calreticulin (CRT), adenosine triphosphate (ATP) and high mobility group box 1 (HMGB1), the main molecular markers of ICD (immunogenic cell death)
ICD↑,
i-ATP↓,
i-HMGB1↓,
ER Stress↑, accumulation of ROS and inducing ERS
ROS↑,
DCells↑, promoted the maturation of dendritic cells (DCs)
CD8+↑, and activation of CD8+T cells
IL12↑, secretion of interleukin-12 (IL-12) and interferon-γ (IFN-γ)
IFN-γ↑,
TGF-β↓, while downregulating transforming growth factor-β (TGF-β) levels

6211- CUR,    The effect of curcumin on hypoxia in the tumour microenvironment as a regulatory factor in cancer
- Review, Var, NA
HIF-1↓, Curcumin, the major component of the rhizomes of Curcuma longa L., reduces HIF-1 levels and function, inhibiting the production of vascular endothelial growth factor (VEGF).
VEGF↓, Curcumin suppresses the HIF-1 pathway under hypoxia, which decreases VEGF expression in both tumour and stromal cells and suppresses angiogenesis.
angioG↓, curcumin efficiently inhibits the angiogenesis of vascular endothelial cells triggered by hypoxia.
RadioS↑, continued interest in curcumin is the molecules’ modulation of initiation, promotion, and progression stages of cancer while concomitantly acting as a radiosensitizer and chemosensitizer for tumours.
ChemoSen↑, Combining cisplatin with curcumin promotes cell apoptosis through the YWHAG pathway and its interaction with HIF-1α, affecting the pentose phosphorylation pathway [
other↝, Cancer patients with hypoxia in their tumours have a poorer prognosis and are at greater risk of metastasis
Apoptosis↑, Curcumin exerts its unique anti-tumour efficacy primarily via pleiotropic functions resulting in apoptosis and decreased tumour cell growth and metastasis
TumCG↓,
TumMeta↓,
BioAv↓, However, due to its low water solubility and low chemical stability, curcumin’s use is limited.
COX2↓, abrogate the proliferation of pancreatic cancer cells through inhibition of COX-2, CD-31, VEGF, and IL-8 and suppression of TGF-β via NF-κB and HIF-1α downregulation
CD31↓,
IL8↓,
TGF-β↓,
NF-kB↓,
JAK2↓, Curcumin application reduced tumourspheres of H460 cells via inhibition of the JAK2/STAT3 signalling pathway
STAT3↓,

6212- CUR,  Rad,    Radiosensitization and Radioprotection by Curcumin in Glioblastoma and Other Cancers
- Review, Var, NA
RadioS↑, Although curcumin can sensitize cancer cells to irradiation, healthy cells are much less sensitive to this effect, and thus, curcumin is thought to be a potent, yet safe anti-cancer agent
*radioP↑, curcumin has been found to possess radioprotective properties, since it can lessen inflammatory toxicities associated with radiotherapy, like dermatitis, mucositis, and myelosuppression
EGFR↓, Curcumin can suppress the gene expression of EGFR, and downregulate the TGF-β pathway, thus leading to inhibition of cancer-associated fibroblasts (CAF)
TGF-β↓,
ROS↑, Curcumin can induce ROS generation and suppress DNA repair machinery, thus leading to increased radiation-induced cell death
P53↑, upregulation of both the expression and activity of p53, regulation of the anti-apoptotic PI3K signaling, and suppression of the activity of NF-κB and COX-2
PI3K↓,
NF-kB↓, curcumin increased radiation-induced apoptotic death primarily through inhibition of the NF-κB signaling pathway
COX2↓,
EMT↓, Curcumin was found to suppress radiation-induced EMT resulting in the inhibition of NSCLC migration and invasion
Hif1a↓, inhibition of the expression of both hypoxia-inducible factor 1-alpha (HIF-1a) and heat shock protein 90 (HSP90) proteins and increase in the levels of ROS
HSP90↓,
mTOR↓, In cervical cancer, curcumin has been studied as a potent mTOR inhibitor when given together with irradiation.
*Catalase↑, 40 rats were exposed to curcumin 1 day before irradiation to 3 consecutive days after irradiation, the levels of antioxidant enzymes, including catalase (CAT), superoxide dismutase (SOD), and malondialdehyde (MDA), were found to be considerably eleva
*SOD↑,
*MDA↑,
*Wound Healing↑, treatment with curcumin stimulated wound healing,
*hepatoP↑, curcumin treatment prior to radiation can prevent liver damages, mainly through the modulation of the NF-κB pathway and reduction of oxidative stress (upregulation of SOD, CAD and GSH levels in the curcumin-treated group)
*NF-kB↓,
*ROS↓,

2688- CUR,    Effects of resveratrol, curcumin, berberine and other nutraceuticals on aging, cancer development, cancer stem cells and microRNAs
- Review, Var, NA - Review, AD, NA
*ROS↓, CUR reduced the production of ROS
*SOD↑, CUR also upregulated the expression of superoxide dismutase (SOD) genes
p16↑, The effects of CUR on gene expression in cancer-associated fibroblasts obtained from breast cancer patients has been examined. CUR increased the expression of the p16INK4A and other tumor suppressor proteins
JAK2↓, CUR decreased the activity of the JAK2/STAT3 pathway
STAT3↓,
CXCL12↓, and many molecules involved in cellular growth and metastasis including: stromal cell-derived factor-1 (SDF-1), IL-6, MMP2, MMP9 and TGF-beta
IL6↓,
MMP2↓,
MMP9↓,
TGF-β↓,
α-SMA↓, These effects reduced the levels of alpha-smooth muscle actin (alpha-SMA) which was attributed to decreased migration and invasion of the cells.
LAMs↓, CUR suppressed Lamin B1 and
DNAdam↑, induced DNA damage-independent senescence in proliferating but not quiescent breast stromal fibroblasts in a p16INK4A-dependent manner.
*memory↑, CUR has recently been shown to suppress memory decline by suppressing beta-site amyloid precursor protein cleaving enzyme 1 (BACE1= Beta-secretase 1, an important gene in AD) expression which is implicated in beta-amyoid pathology in 5xFAD transgenic
*cognitive↑, CUR was found to decrease adiposity and improve cognitive function in a similar fashion as CR in 15-month-old mice.
*Inflam↓, The effects of CUR and CR were positively linked with anti-inflammatory or antioxidant actions
*antiOx↑,
*NO↑, CUR treatment increased nNOS expression, acidity and NO concentration
*MDA↓, CUR treatment resulted in decreased levels of MDA
*ROS↓, CUR treatment was determined to cause reduction of ROS in the AMD-RPEs and protected the cells from H2O2-induced cell death by reduction of ROS levels.
DNMT1↓, CUR has been shown to downregulate the expression of DNA methyl transferase I (DNMT1)
ROS↑, induction of ROS and caspase-3-mediated apoptosis
Casp3↑,
Apoptosis↑,
miR-21↓, CUR was determined to decrease both miR-21 and anti-apoptotic protein expression.
LC3II↓, CUR also induced proteins associated with cell death such as LC3-II and other proteins in U251 cells
ChemoSen↑, The combined CUR and temozolomide treatment resulted in enhanced toxicity in U-87 glioblastoma cells.
NF-kB↓, suppression of NF-kappaB activity
CSCs↓, Dendrosomal curcumin increased the expression of miR-145 and decreased the expression of stemness genes including: NANOG, OCT4A, OCT4B1, and SOX2 [113]
Nanog↓,
OCT4↓,
SOX2↓,
eff↑, A synergistic interaction was observed when emodin and CUR were combined in terms of inhibition of cell growth, survival and invasion.
Sp1/3/4↓, CUR inducing ROS which results in suppression of specificity protein expression (SP1, SP3 and SP4) as well as miR-27a.
miR-27a-3p↓,
ZBTB10↑, downregulation of miR-27a by CUR, increased expression of ZBTB10 occurred
SOX9?, This resulted in decreased SOX9 expression.
ChemoSen↑, CUR used in combination with cisplatin resulted in a synergistic cytotoxic effect, while the effects were additive or sub-additive in combination with doxorubicin
VEGF↓, Some of the effects of CUR treatment are inhibition of NF-κB activity and downstream effector proteins, including: VEGF, MMP-9, XIAP, BCL-2 and Cyclin-D1.
XIAP↓,
Bcl-2↓,
cycD1/CCND1↓,
BioAv↑, Piperine is an alkaloid found in the seeds of black pepper (Piper nigrum) and is known to enhance the bioavailability of several therapeutic agents, including CUR
Hif1a↓, CUR inhibits HIF-1 in certain HCC cell lines and in vivo studies with tumor xenografts. CUR also inhibited EMT by suppressing HIF-1alpha activity in HepG2 cells
EMT↓,
BioAv↓, CUR has a poor solubility in aqueous enviroment, and consequently it has a low bioavailability and therefore low concentrations at the target sites.
PTEN↑, CUR treatment has been shown to result in activation of PTEN, which is a target of miR-21.
VEGF↓, CUR treatment resulted in a decrease of VEGF and activated Akt.
Akt↑,
EZH2↓, CUR also suppressed EZH2 expression by induction of miR-let 7c and miR-101.
NOTCH1↓, The expression of NOTCH1 was inhibited upon EZH2 suppression [
TP53↑, CUR has been shown to activate the TP53/miR-192-5p/miR-215/XIAP pathway in NSCLC.
NQO1↑, CUR can also induce the demethylation of the nuclear factor erythroid-2 (NF-E2) related factor-2 (NRT2) gene which in turn activates (NQO1), heme oxygenase-1 (HO1) and an antioxidant stress pathway which can prevent growth in mouse TRAMP-C1 prostate
HO-1↑,

3582- CUR,  PI,    Therapeutic and Preventive Effects of Piperine and its Combination with Curcumin as a Bioenhancer Against Aluminum-Induced Damage in the Astrocyte Cells
*eff↑, In conclusion, the results of the study showed that the use of different concentrations of piperine, curcumin, and their combination had significantly higher % cell viability on aluminum-induced damage in astrocyte cells compared to the damaged contr
*IL6↓, decrease in the amount of IL-6 and TGF-β cytokines also supported that piperine increased the effectiveness of curcumin.
*TGF-β↓,
*BioAv↑, bioavailability-enhancing property of piperine on curcumin was shown for the first time in the literature.

447- CUR,  OXA,    Curcumin reverses oxaliplatin resistance in human colorectal cancer via regulation of TGF-β/Smad2/3 signaling pathway
- vitro+vivo, CRC, HCT116
p‑p65↓,
Bcl-2↓,
Casp3↑,
EMT↓,
p‑SMAD2↓,
p‑SMAD3↓,
N-cadherin↓,
TGF-β↓,
E-cadherin↑,
TumVol↓,
TumCMig↓,

153- CUR,    Curcumin Inhibits Prostate Cancer Bone Metastasis by Up-Regulating Bone Morphogenic Protein-7 in Vivo
- in-vivo, Pca, C4-2B
PSA↓,
TGF-β↓, down regulation of the expression of TGF-β and an up-regulation of the bone morphogenic protein BMP-2 as a result of curcumin feeding
BMPs↑, BMP2,7
TumMeta↓, Curcumin Inhibits Prostate Cancer Bone Metastasis

123- CUR,    Synthesis of novel 4-Boc-piperidone chalcones and evaluation of their cytotoxic activity against highly-metastatic cancer cells
- in-vitro, Colon, LoVo - in-vitro, Colon, COLO205 - in-vitro, Pca, PC3 - in-vitro, Pca, 22Rv1
NF-kB↓, curcumin analog
ATF3↑, our study showed that ATF3 was up-regulated by curcumin in both LNCaP and C4-2B cells
HO-1↑, Our data confirmed the tumor-inhibitory effects of HMOX-1 gene in prostate cancer cells, which was up-regulated by curcumin treatment.
Wnt↓, Wnt, PIK3/AKT/mTOR, and NF-κB signaling pathways were primarily inhibited by curcumin treatment
Akt↓,
mTOR↓,
PTEN↑, and PTEN dependent cell cycle arrest and apoptosis pathways were found to be elevated.
Apoptosis↑,
TGF-β↓, TGF-β signaling pathway was inhibited by curcumin treatment in androgen-dependent and independent manners.
PPARγ↑, Curcumin was also shown to induce PPAR-γ gene expression and inhibit hepatic stellate cell (HSC) activation by interrupting TGF-β signaling in vitro

124- CUR,    Curcumin-Gene Expression Response in Hormone Dependent and Independent Metastatic Prostate Cancer Cells
- in-vitro, Pca, LNCaP - in-vitro, Pca, C4-2B
TGF-β↓, significantly regulated top canonical pathways highlighted that Transforming growth factor beta (TGF-β), Wingless-related integration site (Wnt), Phosphoinositide 3-kinase/Protein Kinase B/ mammalian target of rapamycin (PIK3/AKT(PKB)/mTOR)
Wnt↓,
PI3k/Akt/mTOR↓,
NF-kB↓, and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) signaling were primarily inhibited
PTEN↑,
Apoptosis↑,
TumCCA↑, Phosphatase and tensin homolog (PTEN) dependent cell cycle arrest and apoptosis pathways were elevated with curcumin treatment.

13- CUR,    Role of curcumin in regulating p53 in breast cancer: an overview of the mechanism of action
- Review, BC, NA
P53↑, upregulated other targets including p53, death receptor (DR-5), JN-kinase, Nrf-2, and peroxisome proliferator-activated receptor γ (PPARγ) factors
DR5↑,
JNK↑,
NRF2↑,
PPARγ↑,
HER2/EBBR2↓, (Her-2, IR, ER-a, and Fas receptor)
IR↓,
ER(estro)↓,
Fas↑,
PDGF↓, (PDGF, TGF, FGF, and EGF)
TGF-β↓,
FGF↓,
EGFR↓,
JAK↓,
PAK↓,
MAPK↓,
ATPase↓, (ATPase, COX-2, and matrix metalloproteinase enzyme [MMP])
COX2↓,
MMPs↓,
IL1↓, inflammatory cytokines (IL-1, IL-2, IL-5, IL-6, IL-8, IL-12, and IL-18)
IL2↓,
IL5↓,
IL6↓,
IL8↓,
IL12↓,
IL18↓,
NF-kB↓,
NOTCH1↓,
STAT1↓,
STAT4↓,
STAT5↓,
STAT3↓,

6663- DFE,    Nutraceuticals of Phoenix dactylifera L.: Physicochemistry, Nutritional Value and Therapeutic Potential
- Review, Nor, NA - Review, AD, NA
*antiOx↑, Date palm products are rich in carbohydrates, dietary fiber, essential minerals, and phenolic and flavonoid compounds, such as gallic acid, catechin, quercetin, and ferulic acid, which underpin their antioxidant and anti-inflammatory properties.
*Inflam↓,
*AntiBio↑, Experimental studies further suggest potential antimicrobial, antihyperlipidemic, antidiabetic, anticancer, anti-arthritic, neuroprotective, hepatoprotective, and gastroprotective effects.
*AntiDiabetic↑,
*AntiCan↑,
*AntiArt↑, biosynthesized AgNPs derived from date seed extracts has been reported to exhibit anti-arthritic activity in experimental models
*neuroP↑,
*hepatoP↑,
*GastroP↑,
*other↝, The mineral composition of date palm fruits (Table 6) reveals potassium as the most abundant mineral, followed by magnesium, calcium, and phosphorus.
*cardioP↑, This mineral profile supports the use of date palm fruit as a functional food for cardiovascular health, particularly in individuals with hypertension, due to its high potassium and low sodium content.
*cognitive↑, Multiple preclinical studies provided evidence that these compounds may enhance brain health and cognitive performance by mitigating oxidative stress and modulating inflammatory mediators, thus alleviating memory impairments and inflammation.
*ROS↓,
*memory↑, reported that date palm extracts were associated with improvements in memory performance, antioxidant enzyme activity, and preservation of neuronal morphology, particularly in the CA1 region of the hippocampus
*other↝, numerous literature have reported that both date fruit and seed extracts may alleviate oxidative stress, subsequently exerting anti-inflammatory, cardioprotective, and metabolic regulatory effects through modulation of related signaling pathways.
*SOD↑, Date fruit extract treatment was also found to restore antioxidant enzyme activities including superoxide dismutase (SOD) and catalase (CAT), and elevated glutathione (GSH) levels, further strengthening its proposed protective role against oxidative
*Catalase↑,
*GSH↑,
*GA↑, rich in phenolic acids and flavonoids, such as gallic acid, catechin, epicatechin, p-coumaric acid, ferulic acid, syringic acid, vanillic acid, quercetin, apigenin, caffeic acid, rutin, and lutein,
*Catechins↑,
*FA↑,
*QC↑,
Api↑,
*CA↑,
*Imm↑, Phoenix dactylifera L. extracts have also been reported to enhance immune function. The high polyphenol content in Phoenix dactylifera L. has been shown to stimulate immune responses
*Phen↑,
*IL1β↓, downregulation of pro-inflammatory mediators, including IL-1β, tumor growth factor (TGF)-β, COX-1, and COX-2, in middle-aged women following chronic consumption of date seed
*TGF-β↓,
*COX1↓,
*COX2↓,
TumCP↓, Phoenix dactylifera L. aqueous-ethanolic extract demonstrated antiproliferative and anti-inflammatory activities against human breast cancer cell lines (MDA-MB-231 and MCF-7)
Casp3↑, seed extracts demonstrated pro-apoptotic effects via caspase-3 activation in MDA‑MB‑231 cells
TumMeta↓, exhibited antiproliferative effects against U87 glioblastoma and MDA‑MB‑231 cells, along with significant inhibition of cell adhesion and migration, indicating potential anti-metastatic properties.
*GutMicro↑, It was suggested that daily consumption of dates may provide fermentable substrates for gut microbiota, thereby reducing toxic protein-derived metabolites.

1607- EA,    Exploring the Potential of Ellagic Acid in Gastrointestinal Cancer Prevention: Recent Advances and Future Directions
- Review, GC, NA
STAT3↓, EA inhibits STAT3 signaling
TumCP↓, EA inhibits cell proliferation, induces apoptosis
Apoptosis↑,
NF-kB↓, inhibiting nuclear factor-kappa B
EMT↓, suppressing epithelial–mesenchymal transition
RadioS↑, In liver cancer, EA exhibits radio-sensitizing effects
antiOx↑, As a potential antioxidant agent,
COX1↓, EA suppresses the expression of several factors, including COX1, COX2, c-myc, snail, and twist1
COX2↓,
cMyc↓,
Snail↓,
Twist↓,
MMP2↓, significantly decreased MMP-2 and MMP-9 expression and activity.
P90RSK↓,
CDK8↓, downregulate CDK8 expression and activity
PI3K↓, inactivating PI3K/Akt signaling
Akt↓,
TumCCA↑, promote cell cycle arrest
Casp8↑, ctivating caspase-8, and lowering proliferating cell nuclear antigen (PCNA) expression,
PCNA↓,
TGF-β↓,
Shh↓, suppression of the Akt, Shh, and Notch pathways, EA can prevent the growth, angiogenesis, and metastasis of pancreatic cancer
NOTCH↓,
IL6↓,
ALAT↓, decreasing liver injury biomarkers such as alanine transaminase (ALT), alkaline phosphatase (ALP), and aspartate aminotransferase (AST)
ALP↓,
AST↓,
VEGF↓,
P21↑,
*toxicity∅, no toxicity was found for a 50% effective dose by the intraperitoneal route inferior to 1 mg/kg/day
*Inflam↓, ncluding anti-inflammatory [10], anti-oxidant [11], anti-allergic [12], and anti-mutagenic [13] properties, as well as potential health advantages like gastroprotective [14], cardioprotective [15], neuroprotective [16, 17], and hepatoprotective [18,
*cardioP↑,
*neuroP↑,
*hepatoP↑,
ROS↑, Exposure to EAs induced apoptosis, accelerated cell cycle arrest, and elevated the generation of reactive oxygen intermediates [59].
*NRF2↓, As a potential antioxidant agent, it scavenges reactive oxygen species (ROS), and by upregulating of Nrf2,
*GSH↑, Moreover, EA increases reduced glutathione (GSH), which is critical for cellular defense against oxidative stress and liver damage,

1605- EA,    Ellagic Acid and Cancer Hallmarks: Insights from Experimental Evidence
- Review, Var, NA
*BioAv↓, Within the gastrointestinal tract, EA has restricted bioavailability, primarily due to its hydrophobic nature and very low water solubility.
antiOx↓, strong antioxidant properties [12,13], anti-inflammatory effects
Inflam↓,
TumCP↓, numerous studies indicate that EA possesses properties that can inhibit cell proliferation
TumCCA↑, achieved this by causing cell cycle arrest at the G1 phase
cycD1/CCND1↓, reduction of cyclin D1 and E levels, as well as to the upregulation of p53 and p21 proteins
cycE/CCNE↓,
P53↑,
P21↑,
COX2↓, notable reduction in the protein expression of COX-2 and NF-κB as a result of this treatment
NF-kB↓,
Akt↑, suppressing Akt and Notch signaling pathways
NOTCH↓,
CDK2↓,
CDK6↓,
JAK↓, suppression of the JAK/STAT3 pathway
STAT3↓,
EGFR↓, decreased expression of epidermal growth factor receptor (EGFR)
p‑ERK↓, downregulated the expression of phosphorylated ERK1/2, AKT, and STAT3
p‑Akt↓,
p‑STAT3↓,
TGF-β↓, downregulation of the TGF-β/Smad3
SMAD3↓,
CDK6↓, EA demonstrated the capacity to bind to CDK6 and effectively inhibit its activity
Wnt/(β-catenin)↓, ability of EA to inhibit phosphorylation of EGFR
Myc↓, Myc, cyclin D1, and survivin, exhibited decreased levels
survivin↓,
CDK8↓, diminished CDK8 level
PKCδ↓, EA has demonstrated a notable downregulatory impact on the expression of classical isoenzymes of the PKC family (PKCα, PKCβ, and PKCγ).
tumCV↓, EA decreased cell viability
RadioS↑, further intensified when EA was combined with gamma irradiation.
eff↑, EA additionally potentiated the impact of quercetin in promoting the phosphorylation of p53 at Ser 15 and increasing p21 protein levels in the human leukemia cell line (MOLT-4)
MDM2↓, finding points to the ability of reduced MDM2 levels
XIAP↓, downregulation of X-linked inhibitor of apoptosis protein (XIAP).
p‑RB1↓, EA exerted a decrease in phosphorylation of pRB
PTEN↑, EA enhances the protein phosphatase activity of PTEN in melanoma cells (B16F10)
p‑FAK↓, reduced phosphorylation of focal adhesion kinase (FAK)
Bax:Bcl2↑, EA significantly increases the Bax/Bcl-2 rati
Bcl-xL↓, downregulates Bcl-xL and Mcl-1
Mcl-1↓,
PUMA↑, EA also increases the expression of Bcl-2 inhibitory proapoptotic proteins PUMA and Noxa in prostate cancer cells
NOXA↑,
MMP↓, addition to the reduction in MMP, the release of cytochrome c into the cytosol occurs in pancreatic cancer cells
Cyt‑c↑,
ROS↑, induction of ROS production
Ca+2↝, changes in intracellular calcium concentration, leading to increased levels of EndoG, Smac/DIABLO, AIF, cytochrome c, and APAF1 in the cytosol
Endoglin↑,
Diablo↑,
AIF↑,
iNOS↓, decreased expression of Bcl-2, NF-кB, and iNOS were observed after exposure to EA at concentrations of 15 and 30 µg/mL
Casp9↑, increase in caspase 9 activity in EA-treated pancreatic cancer cells PANC-1
Casp3↑, EA-induced caspase 3 activation and PARP cleavage in a dose-dependent manner (10–100 µmol/L)
cl‑PARP↑,
RadioS↑, EA sensitizes and reduces the resistance of breast cancer MCF-7 cells to apoptosis induced by γ-radiation
Hif1a↓, EA reduced the expression of HIF-1α
HO-1↓, EA significantly reduced the levels of two isoforms of this enzyme, HO-1, and HO-2, and increased the levels of sEH (Soluble epoxide hydrolase) in LnCap
HO-2↓,
SIRT1↓, EA-induced apoptosis was associated with reduced expression of HuR and Sirt1
selectivity↑, A significant advantage of EA as a potential chemopreventive, anti-tumor, or adjuvant therapeutic agent in cancer treatment is its relative selectivity
Dose∅, EA significantly reduced the viability of cancer cells at a concentration of 10 µmol/L, while in healthy cells, this effect was observed only at a concentration of 200 µmol/L
NHE1↓, EA had the capacity to regulate cytosolic pH by downregulating the expression of the Na+/H+ exchanger (NHE1)
Glycolysis↓, led to intracellular acidification with subsequent impairment of glycolysis
GlucoseCon↓, associated with a decrease in the cellular uptake of glucose
lactateProd↓, notable reduction in lactate levels in supernatant
PDK1?, inhibit pyruvate dehydrogenase kinase (PDK) -bind and inhibit PDK3
PDK1?,
ECAR↝, EA has been shown to influence extracellular acidosis
COX1↓, downregulation of cancer-related genes, including COX1, COX2, snail, twist1, and c-Myc.
Snail↓,
Twist↓,
cMyc↓,
Telomerase↓, EA, might dose-dependently inhibit telomerase activity
angioG↓, EA may inhibit angiogenesis
MMP2↓, EA demonstrated a notable reduction in the secretion of matrix metalloproteinase (MMP)-2 and MMP-9.
MMP9↓,
VEGF↓, At lower concentrations (10 and 20 μM), EA led to a substantial increase in VEGF levels. However, at higher doses (40 and 100 μM), a notable reduction in VEGF
Dose↝, At lower concentrations (10 and 20 μM), EA led to a substantial increase in VEGF levels. However, at higher doses (40 and 100 μM), a notable reduction in VEGF
PD-L1↓, EA downregulated the expression of the immune checkpoint PD-L1 in tumor cells
eff↑, EA might potentially enhance the efficacy of anti-PD-L1 treatment
SIRT6↑, EA exhibited statistically significant upregulation of sirtuin 6 at the protein level in Caco2 cells
DNAdam↓, increase in DNA damage

1618- EA,    A comprehensive review on Ellagic acid in breast cancer treatment: From cellular effects to molecular mechanisms of action
- Review, BC, NA
TumCCA↑, suppresses the growth of BC cells by arresting the cell cycle in the G0/G1 phase,
TumCMig↓, suppresses migration, invasion, and metastatic
TumCI↓,
TumMeta↓,
Apoptosis↑, stimulates apoptosis in MCF-7 cells via TGF-β/Smad3 signaling axis
TGF-β↓,
SMAD3↓,
CDK6↓, inhibits CDK6 that is important in cell cycle regulation,
PI3K↓, inhibits the PI3K/AKT pathway
Akt↓,
angioG↓,
VEGFR2↓, reduces VEGFR-2 tyrosine kinase activity
MAPK↓,
NEDD9↓, downregulated protein 9 (NEDD-9)
NF-kB↓, EA suppressed NF-κB precursor protein p105
eff↑, They showed that the encapsulation of EA in biodegradable polymeric nanoparticles would improve the bioavailability after oral administration and also enhance the anticancer properties
eff↑, Chitosan nanoparticles and EA with high anticancer efficacy could be a suitable therapeutic strategy
RadioS↑, showed that the synergistic effect of EA combined with radiotherapy/chemotherapy resulted in increased DNA damage and apoptosis as well as decreased levels of MGMT expression
ChemoSen↑,
DNAdam↑,
eff↑, combination of Paclitaxel and EA has shown promise in inhibiting tumor growth and metastasis in experimental BC models.
*toxicity∅, 630 mg/kg is the LD50 of EA in the rat population.
*toxicity∅, no-observed adverse effect level of EA is 2000 mg/kg body weight

1110- EA,  GEM,    Ellagic Acid Resensitizes Gemcitabine-Resistant Bladder Cancer Cells by Inhibiting Epithelial-Mesenchymal Transition and Gemcitabine Transporters
- vitro+vivo, Bladder, NA
TGF-β↓,
SMAD2↓,
SMAD3↓,
SMAD4↓,

1072- EGCG,    Epigallocatechin gallate (EGCG) suppresses epithelial-Mesenchymal transition (EMT) and invasion in anaplastic thyroid carcinoma cells through blocking of TGF-β1/Smad signaling pathways
- in-vitro, Thyroid, 8505C
EMT↓,
TumCI↓,
TumCMig↓,
TGF-β↓,
p‑SMAD2↓,
p‑SMAD3↓,
SMAD4↓,

26- EGCG,  QC,  docx,    Green tea and quercetin sensitize PC-3 xenograft prostate tumors to docetaxel chemotherapy
- vitro+vivo, Pca, PC3
BAD↓,
cl‑PARP↑,
Casp7↑,
IκB↓,
Ki-67↓,
VEGF↓,
EGFR↓,
FGF↓,
TGF-β↓,
TNF-α↓,
SCF↓,
Bax:Bcl2↑,
NF-kB↓,
chemoP↑, This study provides a novel regimen to enhance the therapeutic effect of Doc in a less-toxic manner and reduce its risk of side effects in treatment of CRPC.
ChemoSen↑, GT and Q with LD Doc significantly enhanced the potency of Doc 2-fold and reduced tumor growth by 62 % compared to LD Doc in 7-weeks intervention.
TumVol↓,

6784- EGCG,    Dietary (−)-Epigallocatechin Gallate (EGCG): State-of-the-Art Advances in Bioactivities, Bioavailability Enhancement Strategies, and Applications in Nutrition and Health
- Review, Nor, NA
*antiOx↑, bioactivities of EGCG, including its antioxidant, anti-inflammatory, anticancer, cardiovascular protective, metabolic regulatory, neuroprotective, gut microbiota-modulating, and antimicrobial properties.
*Inflam↓,
*AntiCan↑,
*cardioP↑,
*neuroP↑,
*GutMicro↑,
*AntiBio↑,
*ROS↓, Figure 1, anti inflammatory
*TNF-α↓,
*IL6↓,
TumCP↓,
*LDL↓, cardioprotective
*NO↓,
*Obesity↓, Metabolic syndrome
*p‑tau↓, nervous system
*Aβ↓,
*NRF2↑, , EGCG has been shown to activate the Keap1/P62/Nrf2 signaling pathway,
*SOD↑, upregulation of endogenous antioxidant enzymes, such as superoxide dismutase, catalase, and glutathione peroxidase, indirectly diminishing the levels of intracellular oxygen free radicals
*Catalase↑,
*GPx↑,
*NLRP3↓, EGCG also restores autophagy levels, suppresses the activation of the NLRP3 inflammasome by inhibiting the mammalian target of rapamycin signaling pathway
*mTOR↓,
TumCCA↑, Cancer: induce cell cycle arrest and inhibit tumor cell proliferation
NRF2↓, EGCG inhibits CCL5-stimulated lung cancer cell proliferation by down-regulating Nrf2 expression
Apoptosis↑, Inducing Apoptosis in Cancer Cells
SIRT1↓, EGCG activates the mitochondrial apoptotic pathway by downregulating SIRT1 expression to modulate the SIRT1-p53 axis
miR-25-5p↓, In breast cancer, EGCG induces apoptosis by inhibiting miR-25 expression and elevating PARP, pre-caspase-3 and pre-caspase-9 protein levels
PARP↑,
Casp3↑,
Casp9↑,
ER Stress↑, in multiple myeloma, EGCG promotes apoptosis by activating the endoplasmic reticulum stress pathway
TumAuto↑, EGCG induces autophagic cell death in breast cancer cells by retaining YAP1 in the cytoplasm and promoting the assembly of the CHMP2B-VPS4B complex
EMT↓, EGCG has been demonstrated to inhibit EMT, invasion, and migration by blocking the TGFβ/Smad signaling pathway
TumCI↓,
TumCMig↓,
TGF-β↓,
Smad1↓,
STAT3↓, EGCG can directly bind to STAT3, reducing nuclear localization and inhibiting the transcription of PLXNC1.
VEGF↓, widely believed that EGCG can block this process by reducing the expression of vascular endothelial growth factor, a key factor in angiogenesis,
angioG↓, The inhibition of angiogenic mimicry by EGCG through the Twist/VE-calmodulin/AKT pathway has also been demonstrated in prostate cancer cells
Imm↑, Acting as an Immunomodulator
EGFR↓, EGCG possesses the ability to interact with EGFR and inhibit activity, strengthening the anticancer evidence for EGCG
*GutMicro↑, EGCG can regulate the balance of gut flora. For example, EGCG can inhibit the growth of harmful bacteria such as Escherichia coli and Salmonella, while promoting the proliferation of probiotics like Bifidobacterium and Lactobacillus
*Bacteria↓, Antibacterial and Antiviral Properties of EGCG
*AntiViral↑,
*BioAv↓, EGCG, its low bioavailability in the human body limits clinical efficacy.
*BioAv↑, Nanotechnology strategy of EGCG.
*eff↑, Co-encapsulation assay of EGCG with quercetin shows that the two synergistically enhanced the antioxidant capacity of EGCG
*BioAv↑, Combining EGCG with resveratrol increases its solubility and significantly improves its absorption in the small intestine.
eff↑, combination of EGCG and curcumin inhibits the activity of metabolic enzymes, reduces the rate of metabolism in the liver and enhances its antitumor efficacy
ChemoSen↑, synergistic effects of EGCG combined with chemotherapeutic agents such as 5-fluorouracil, celecoxib, cisplatin, and tamoxifen have also been reported
*toxicity↝, The European Food Safety Authority notes in scientific opinion that daily oral doses of 800 mg or higher of EGCG represent a common starting point for observed cases of liver injury

6820- EMD,    The Health Benefits of Emodin, a Natural Anthraquinone Derived from Rhubarb—A Summary Update
- Review, Nor, NA - Review, Arthritis, NA - Review, AD, NA
*diuretic↑, Emodin has a wide range of biological activities, including diuretic, antibacterial, antiulcer, anti-inflammatory, anticancer and antinociceptive.
*Bacteria↓,
*Inflam↓,
AntiCan↑,
TumCP↓, emodin inhibits processes of neoplasia at the stages of proliferation, invasion and angiogenesis.
TumCI↓,
angioG↓,
*toxicity↓, The results showed that administration of emodin at the doses of 20, 40, and 80 mg/kg for 12 weeks is safe and did not cause any pathophysiological disorders in major organs in mammals.
IFN-γ↑, more interferon gamma (IFN-γ), interleukin (IL)-12 and reactive oxygen species (ROS) and less IL-6, tumor necrosis factor alpha (TNF-α) and transforming growth factor beta1 (TGF-β1) in he alveolar cavity in the emodin group than those in the control
IL12↑,
ROS↑, In vitro, emodin at the dose of 20 μM had no effect on cell viability in HL-60N1, but increased ROS and decreased autophagy, and thus induced apoptosis in HL-60N2
TNF-α↓,
TNF-α↓,
TGF-β↓,
MAPK↓, Antitumor properties of emodin are associated with inhibiting the activity of tyrosine kinases, such as mitogen-activated protein kinase (MAPK), protein kinase C (PKC), factor kappa-light-chain-enhancer of activated B cells (NF-κB)
PKCδ↓,
NF-kB↓,
HER2/EBBR2↓, emodin suppresses the activity of HER-2/neu tyrosine kinase [55]; whereas, in colon cancer cells, emodin inhibits phosphorylation of vascular endothelial growth factor (VEGF)
VEGF↓,
DNAdam↑, Another antiproliferative mechanism of emodin activity involves induction of DNA damage by the ROS, whose concentration is considerably increased in the cells treated with this anthraquinone.
Necroptosis↑, emodin induces necroptosis in the cells of renal cancer (RCC), which is resistant to conventional cancer therapy, such as chemotherapy or radiotherapy.
Glycolysis↓, and also inhibits glycolysis by downregulation of GLUT1 through ROS-mediated inactivation of the phosphoinositide 3-kinases (PI3K)/AKT signaling pathway.
GLUT1↓,
PI3K↓,
Akt↓,
Casp9↑, increasing active caspase-9, active caspase-3, and bcl-2-like protein 4 (Bax) levels and downregulating Bcl-2.
Casp3↑,
BAX↑,
Bcl-2↓,
eff↑, Li et al. [61] revealed that a bifunctional molecule of β-dihydro-artemisinin-emodin has high antiproliferative activity (suppressing Ki-67 expression),
MMP2↓, Emodin effectively inhibits the expression of the angiogenic-related NF-kB factor, as well as its regulatory factors, including VEGF, MMP-2, MMP-9.
MMP9↓,
eff↑, Combinatorial therapy with emodin and thymoquinone was also efficient in attenuating migration of MCF-7 breast cancer cells, inducing apoptosis, inhibiting cell proliferation, while enhancing cytotoxicity
ChemoSen↑, For example, combination therapy using emodin and doxorubicin sensitize breast cancer cells to doxorubicin by inhibition of proliferation in the DNA damage pathway
P-gp↓, It was demonstrated that emodin downregulated Pgp expression, and enhanced cisplatin-induced apoptosis and DNA damage in the cancer cells
SREBP2↓, suppressing the cholesterol biosynthesis (inhibition the activity of SREBP-2 protein) and inhibiting the expression of the AKT.
eff↑, emodin combined with berberine significantly inhibited the activity of salt-inducible kinases 3 (SIK3), belonging to the AMPK-related kinases, which elevated expressions in breast cancer cells contributing to tumorigenesis.
*other↝, emodin has therapeutic potential for the treatment of various kinds of inflammation, such as pancreatitis, asthma, arthritis, atherosclerosis, myocarditis, glomerulonephritis and Alzheimer’s disease.
*COX2↓, Therapeutic properties of emodin in the treatment of joint inflammation are also associated with inhibition of expression of VEGF, cyclooxygenase 2 (COX-2), hypoxia-inducible factor 1 (HIF-1)α and histone deacetylase (HDAC).
*Hif1a↓,
*HDAC↓,
*tau↓, Emodin effectively prevents abnormal aggregation of tau proteins in PHFs
*PKCδ↑, emodin improved cognitive functions by activating the protein kinase C signaling pathway (PKC), attenuating oxidative stress and inflammatory response in mice with Alzheimer’s disease.
*ROS↓,
*Inflam↓,
AntiAg?,

1322- EMD,    The versatile emodin: A natural easily acquired anthraquinone possesses promising anticancer properties against a variety of cancers
- Review, Var, NA
Apoptosis↑,
TumCP↓,
ROS↑,
TumAuto↑,
EMT↓,
TGF-β↓,
DNAdam↑,
ER Stress↑,
TumCCA↑,
ATP↓,
NF-kB↓,
CYP1A1↑,
STAC2↓,
JAK↓,
PI3K↓,
Akt↓,
MAPK↓,
FASN↓,
HER2/EBBR2↓,
ChemoSen↑, DOX combined with emodin can improve the sensitivity of MDA-MB-231 and MCF-7 cells to chemotherapy
eff↑, emodin was reported to increase the anti-proliferative effect of an EGFR inhibitor (afatinib) against PC through downregulation of EGFR by promoting STAT3
ChemoSen↑, gemcitabine combined with emodin increased cell death
angioG↓,
VEGF↓,
MMP2↓,
eNOS↓,
FOXD3↑,
MMP9↓,
TIMP1↑,

1246- EMD,    Emodin reduces Breast Cancer Lung Metastasis by suppressing Macrophage-induced Breast Cancer Cell Epithelial-mesenchymal transition and Cancer Stem Cell formation
- in-vivo, BC, NA
TGF-β↓, Emodin suppressed TGF-β1 production in breast cancer cells
EMT↓,
CSCs↓,

6580- EU,    Eurycomanone Blocks TGF-β1-Induced Epithelial-to-Mesenchymal Transition, Migration, and Invasion Pathways in Human Non-Small Cell Lung Cancer Cells by Targeting Smad and Non-Smad Signaling
- in-vitro, Lung, A549 - in-vitro, Lung, Calu-1
TumCMig↓, ECN significantly suppressed the migration of both TGF-β1-induced A549 and Calu-1 cells.
MMP2↓, decreased the secretion of MMP-2 from these cancer cells.
EMT↓, ECN Suppresses TGF-β1-Induced Epithelial-to-Mesenchymal Transition of NSCLC Cells
E-cadherin↑, ECN significantly restored the expression of E-cadherin by inhibiting the Akt signaling pathway.
Akt↓,
N-cadherin↓, in Calu-1, ECN reduced the aggressive phenotype by decreasing the expression of the mesenchymal protein N-cadherin and inhibiting the TGF-β1/Smad pathway.
TGF-β↓,
Smad1↓,

2839- FIS,    Dietary flavonoid fisetin for cancer prevention and treatment
- Review, Var, NA
DNAdam↑, Fisetin induced DNA fragmentation, ROS generation, and apoptosis in NCI-H460 cells via a reduction in Bcl-2 and increase in Bax expression
ROS↑,
Apoptosis↑,
Bcl-2↓,
BAX↑,
cl‑Casp9↑, Fisetin treatment increased cleavage of caspase-9 and caspase-3 thereby increasing caspase-3 activation
cl‑Casp3↑,
Cyt‑c↑, leading to cytochrome-c release
lipid-P↓, Fisetin (25 mg/kg body weight) decreased histological lesions and levels of lipid peroxidation and modulated the enzymatic and nonenzymatic anti-oxidants in B(a)P-treated Swiss Albino mice
TumCG↓, We observed that fisetin treatment (5–20 μM) inhibits cell growth and colony formation in A549 NSC lung cancer cells.
TumCA↓, Another study showed that fisetin inhibits adhesion, migration, and invasion in A549 lung cancer cells by downregulating uPA, ERK1/2, and MMP-2
TumCMig↓,
TumCI↓,
uPA↓,
ERK↓,
MMP9↓,
NF-kB↓, Treatment with fisetin also decreased the nuclear levels of NF-kB, c-Fos, c-Jun, and AP-1 and inhibited NF-kB binding.
cFos↓,
cJun↓,
AP-1↓,
TumCCA↑, Our laboratory has previously shown that treatment of LNCaP cells with fisetin caused inhibition of PCa by G1-phase cell cycle arrest
AR↓, inhibited androgen signaling and tumor growth in athymic nude mice
mTORC1↓, induced autophagic cell death in PCa cells through suppression of mTORC1 and mTORC2
mTORC2↓,
TSC2↑, activated the mTOR repressor TSC2, commonly associated with inhibition of Akt and activation of AMPK
EGF↓, Fisetin also inhibits EGF and TGF-β induced YB-1 phosphorylation and EMT in PCa cells
TGF-β↓,
EMT↓, Fisetin also inhibits EGF and TGF-β induced YB-1 phosphorylation and EMT in PCa cells
P-gp↓, decrease the P-gp protein in multidrug resistant NCI/ADR-RES cells.
PI3K↓, Fisetin also inhibited the PI3K/AKT/NFkB signaling
Akt↓,
mTOR↓, Fisetin inhibited melanoma progression in a 3D melanoma skin model with downregulation of mTOR, Akt, and upregulation of TSC
eff↑, combinational treatment study of melatonin and fisetin demonstrated enhanced antitumor activity of fisetin
ROS↓, Fisetin inhibited ROS and augmented NO generation in A375 melanoma cells
ER Stress↑, induction of ER stress evidenced by increased IRE1α, XBP1s, ATF4, and GRP78 levels in A375 and 451Lu cells.
IRE1↑,
ATF4↑,
GRP78/BiP↑,
ChemoSen↑, combination of fisetin with sorafenib effectively inhibited EMT and augmented the anti-metastatic potential of sorafenib by reducing MMP-2 and MMP-9 proteins in melanoma cell xenografts
CDK2↓, Fisetin (0–60 μM) was shown to inhibit activity of CDKs dose-dependently leading to cell cycle arrest in HT-29 human colon cancer cells
CDK4↓, Fisetin treatment decreased activities of CDK2 and CDK4 via decreased levels of cyclin-E, cyclin-D1 and increase in p21 (CIP1/WAF1) levels.
cycE/CCNE↓,
cycD1/CCND1↓,
P21↑,
COX2↓, fisetin (30–120 μM) induces apoptosis in colon cancer cells by inhibiting COX-2 and Wnt/EGFR/NF-kB -signaling pathways
Wnt↓,
EGFR↓,
β-catenin/ZEB1↓, Fisetin treatment inhibited Wnt/EGFR/NF-kB signaling via downregulation of β-catenin, TCF-4, cyclin D1, and MMP-7
TCF-4↓,
MMP7↓,
RadioS↑, fisetin treatment was found to radiosensitize human colorectal cancer cells which are resistant to radiotherapy
eff↑, Combined treatment of fisetin with NAC increased cleaved caspase-3, PARP, reduced mitochondrial membrane potential with induction of caspase-9 in COLO25 cells

4027- FulvicA,    Mummy Induces Apoptosis Through Inhibiting of Epithelial-Mesenchymal Transition (EMT) in Human Breast Cancer Cells
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, MCF7 - in-vitro, Nor, MCF10
tumCV↓, MDA-MB-231 showed more sensitivity than the MCF-7 cell line to the anticancer activity of mummy,
selectivity↑, while mummy did not exhibit significant cell cytotoxicity against human normal cells (MCF-10A).
TGF-β↓, gene expression profile demonstrated a significant decrease in TGF-β1, TGF-βR1, TWIST1, NOTCH1, CTNNB1, SRC along with an increase in E-cadherin mRNA levels in mummy treated cells compared to the untreated control group
Twist↓,
NOTCH1↓,
CTNNB1↓,
Src↓,
E-cadherin↑,
EMT↓, Mummy triggers inhibition of EMT and metastasis in breast cancer cells mainly through the downregulation of TGFβ1 activity
TumMeta↓,
BioAv↑, water-soluble non-toxic and inexpensive compound, can be consumed as a part of the daily diet

805- GAR,  Cisplatin,  PacT,    Garcinol Exhibits Anti-Neoplastic Effects by Targeting Diverse Oncogenic Factors in Tumor Cells
- Review, NA, NA
ERK↓, ERK1/2
PI3K/Akt↓,
Wnt/(β-catenin)↓,
STAT3↓,
NF-kB↓,
ChemoSen↑, cisplatin or paclitaxel, in the presence of garcinol can lead to a significant increase in the treatment outcome
COX2↓,
Casp3↑,
Casp9↑,
BAX↑,
Bcl-2↓,
VEGF↓,
TGF-β↓,
HATs↓,
E-cadherin↑,
Vim↓,
Zeb1↓,
ZEB2↓,
Let-7↑,
MMP9↓,
TumCCA↑, cycle arrest at G0/G1 phase
ROS↑,
MMP↓,
IL6↓,
NOTCH1↓,

817- GAR,    Garcinol inhibits esophageal cancer metastasis by suppressing the p300 and TGF-β1 signaling pathways
- vitro+vivo, SCC, KYSE150 - vitro+vivo, SCC, KYSE450
HATs↓, Garcinol, a natural compound extracted from Gambogic genera, is a histone acetyltransferase (HAT) inhibitor
TumCCA↑,
Apoptosis↑,
TumCMig↓,
TumCI↓,
CBP↓,
p300↓,
TGF-β↓, suppressed TGF-β1-activated Smad and non-Smad pathway
Ki-67↓,
SMAD2↓,
SMAD3↓,

822- GAR,    Garcinol, a Polyisoprenylated Benzophenone Modulates Multiple Proinflammatory Signaling Cascades Leading to the Suppression of Growth and Survival of Head and Neck Carcinoma
- vitro+vivo, HNSCC, NA
ROS↑, generation of reactive oxygen species is involved in STAT3 inhibitory effect of garcinol.
STAT3↓,
cSrc↓,
JAK1↓,
JAK2↓,
NF-kB↓,
TGF-β↓,
TumCG↓,


Showing Research Papers: 1 to 50 of 89
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* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 89

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↓, 2,   antiOx↑, 1,   ATF3↑, 1,   CYP1A1↑, 1,   Ferroptosis↑, 1,   GPx4↓, 1,   H2O2↑, 1,   HO-1↓, 1,   HO-1↑, 2,   HO-2↓, 1,   ICD↑, 1,   lipid-P↓, 1,   NOX4↓, 1,   NQO1↑, 1,   NRF2↓, 1,   NRF2↑, 1,   NRF2↝, 1,   ROS↓, 2,   ROS↑, 20,   SOD2↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

AIF↑, 2,   ATP↓, 1,   i-ATP↓, 1,   CDC25↓, 2,   EGF↓, 1,   MEK↓, 1,   p‑MEK↓, 1,   MMP↓, 8,   mtDam↑, 2,   XIAP↓, 3,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

12LOX↓, 2,   ALAT↓, 1,   AMPK↑, 2,   cMyc↓, 4,   ECAR↝, 1,   FASN↓, 1,   GlucoseCon↓, 2,   Glycolysis↓, 3,   H2S↑, 1,   HK2↓, 1,   IR↓, 1,   lactateProd↓, 2,   PDK1?, 2,   PI3K/Akt↓, 1,   PI3k/Akt/mTOR↓, 1,   PKM2↓, 1,   PPARγ↑, 3,   SIRT1↓, 2,   SIRT1↑, 1,   SREBP2↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 14,   Akt↑, 2,   p‑Akt↓, 2,   Apoptosis↑, 18,   BAD↓, 2,   Bak↑, 1,   BAX↑, 10,   Bax:Bcl2↑, 2,   Bcl-2↓, 8,   Bcl-xL↓, 3,   Casp↑, 1,   Casp2↑, 1,   Casp3↓, 1,   Casp3↑, 12,   cl‑Casp3↑, 1,   Casp7↑, 1,   Casp8↑, 5,   Casp9↑, 8,   cl‑Casp9↑, 1,   CBP↓, 1,   p‑Chk2↑, 1,   Cyt‑c↑, 7,   Diablo↑, 1,   DR5↑, 3,   FADD↑, 1,   Fas↑, 7,   FasL↑, 1,   Ferroptosis↑, 1,   IAP1↓, 1,   iNOS↓, 1,   JNK↓, 1,   JNK↑, 4,   MAPK↓, 7,   MAPK↑, 1,   Mcl-1↓, 3,   MDM2↓, 2,   Myc↓, 1,   Necroptosis↑, 1,   NOXA↑, 1,   oncosis↑, 1,   p27↑, 1,   p38↑, 2,   PUMA↑, 1,   survivin↓, 3,   Telomerase↓, 1,  

Kinase & Signal Transduction(tgid=6) ⓘ

cSrc↓, 1,   FOXD3↑, 1,   HER2/EBBR2↓, 3,   miR-25-5p↓, 1,   PAK↓, 1,   SOX9?, 1,   Sp1/3/4↓, 1,   TSC2↑, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

cJun↓, 1,   EZH2↓, 1,   HATs↓, 2,   miR-145↑, 1,   miR-21↓, 1,   miR-27a-3p↓, 1,   other↓, 1,   other↝, 1,   tumCV↓, 2,  

Protein Folding & ER Stress(tgid=8) ⓘ

i-CRT↓, 1,   ER Stress↑, 8,   GRP78/BiP↓, 1,   GRP78/BiP↑, 2,   HSP70/HSPA5↓, 1,   HSP90↓, 2,   IRE1↑, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

Beclin-1↑, 1,   LC3II↓, 1,   LC3II↑, 1,   TumAuto↑, 6,  

DNA Damage & Repair(tgid=10) ⓘ

ATM↑, 1,   p‑ATM↑, 1,   p‑ATR↑, 1,   p‑CHK1↑, 1,   DNAdam↓, 1,   DNAdam↑, 10,   DNMT1↓, 1,   HR↓, 1,   p16↑, 2,   P53↑, 6,   p‑P53↑, 1,   PARP↑, 2,   cl‑PARP↑, 5,   PCNA↓, 1,   RAD51↓, 1,   SIRT6↑, 1,   TP53↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK1↓, 1,   CDK2↓, 4,   CDK4↓, 4,   CycB/CCNB1↓, 1,   CycB/CCNB1↑, 1,   cycD1/CCND1↓, 6,   cycE/CCNE↓, 5,   cycE1↓, 1,   P21↑, 5,   RB1↑, 1,   p‑RB1↓, 1,   TumCCA↑, 16,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

CD24↓, 1,   CDK8↓, 2,   cFos↓, 1,   cMET↓, 1,   CSCs↓, 3,   CTNNB1↓, 1,   EMT↓, 15,   EMT↑, 2,   ERK↓, 6,   p‑ERK↓, 2,   FGF↓, 2,   FOXO3↑, 1,   GSK‐3β↑, 1,   HH↓, 1,   Let-7↑, 1,   mTOR↓, 9,   mTORC1↓, 1,   mTORC2↓, 1,   Nanog↓, 1,   NOTCH↓, 2,   NOTCH1↓, 5,   OCT4↓, 2,   p300↓, 1,   P90RSK↓, 1,   PI3K↓, 11,   PTEN↑, 4,   RAS↓, 1,   SCF↓, 1,   Shh↓, 1,   SOX2↓, 1,   Src↓, 2,   STAT1↓, 1,   STAT3↓, 9,   p‑STAT3↓, 2,   STAT4↓, 1,   STAT5↓, 1,   TCF-4↓, 1,   TumCG↓, 4,   Wnt↓, 4,   Wnt/(β-catenin)↓, 3,   ZFX↓, 1,  

Migration(tgid=13) ⓘ

AntiAg?, 1,   AP-1↓, 1,   ATPase↓, 1,   AXL↓, 1,   Ca+2↑, 5,   Ca+2↝, 1,   CAFs/TAFs↓, 1,   CD31↓, 1,   CDK4/6↓, 1,   CXCL12↓, 1,   E-cadherin↑, 5,   FAK↓, 3,   p‑FAK↓, 1,   fascin↓, 1,   Fibrosis↓, 1,   ITGB1↑, 1,   Ki-67↓, 4,   LAMs↓, 1,   MMP1↓, 1,   MMP13↓, 1,   MMP2↓, 11,   MMP3↓, 1,   MMP7↓, 1,   MMP9↓, 12,   MMPs↓, 2,   N-cadherin↓, 2,   NCAM↑, 1,   NEDD9↓, 1,   PDGF↓, 1,   PKCδ↓, 2,   Rho↓, 1,   ROCK1↓, 1,   Slug↓, 1,   Smad1↓, 2,   SMAD2↓, 4,   p‑SMAD2↓, 5,   SMAD3↓, 7,   p‑SMAD3↓, 3,   SMAD4↓, 5,   Snail?, 1,   Snail↓, 3,   STAC2↓, 1,   TGF-β↓, 45,   TIMP1↓, 1,   TIMP1↑, 1,   TIMP2↓, 1,   TIMP2↑, 1,   TumCA↓, 1,   TumCI↓, 11,   TumCMig↓, 12,   TumCP↓, 14,   TumMeta↓, 9,   Twist↓, 5,   uPA↓, 4,   Vim↓, 2,   Zeb1↓, 2,   ZEB2↓, 2,   α-SMA↓, 2,   β-catenin/ZEB1↓, 3,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 9,   ATF4↑, 1,   ECM/TCF↓, 1,   EGFR↓, 7,   Endoglin↑, 1,   eNOS↓, 1,   HIF-1↓, 3,   Hif1a↓, 6,   KDR/FLK-1↓, 1,   NO↓, 1,   VEGF↓, 15,   VEGFR2↓, 2,   ZBTB10↑, 1,  

Barriers & Transport(tgid=15) ⓘ

GLUT1↓, 2,   NHE1↓, 1,   P-gp↓, 2,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

CD4+↓, 1,   COX1↓, 2,   COX2↓, 11,   DCells↑, 1,   i-HMGB1↓, 1,   IFN-γ↑, 2,   p‑IKKα↓, 1,   IL1↓, 3,   IL10↓, 1,   IL12↓, 1,   IL12↑, 2,   IL18↓, 1,   IL2↓, 1,   IL4↓, 1,   IL5↓, 1,   IL6↓, 6,   IL8↓, 2,   Imm↑, 1,   Inflam↓, 3,   IκB↓, 1,   JAK↓, 3,   JAK1↓, 1,   JAK2↓, 3,   M2 MC↓, 1,   MCP1↓, 1,   MIP2↓, 1,   NF-kB↓, 22,   NF-kB↑, 1,   p65↓, 1,   p‑p65↓, 1,   PD-L1↓, 1,   PGE2↓, 2,   PSA↓, 1,   TNF-α↓, 6,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

AR↓, 1,   CDK6↓, 5,   CDK6↑, 1,   ER(estro)↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 4,   BioAv↑, 3,   ChemoSen↑, 16,   Dose↝, 2,   Dose∅, 1,   eff↑, 23,   Half-Life↝, 1,   RadioS↑, 9,   selectivity↑, 4,  

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 1,   ALP↓, 1,   AR↓, 1,   AST↓, 1,   BMPs↑, 1,   E6↓, 1,   E7↓, 1,   EGFR↓, 7,   EZH2↓, 1,   HER2/EBBR2↓, 3,   IL6↓, 6,   Ki-67↓, 4,   Myc↓, 1,   PD-L1↓, 1,   PSA↓, 1,   TP53↑, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 4,   AntiTum↑, 1,   chemoP↑, 1,   RenoP↑, 1,   TumVol↓, 2,  

Infection & Microbiome(tgid=24) ⓘ

CD8+↑, 1,  

Ingredients & Constituents(tgid=25) ⓘ

Api↑, 1,  
Total Targets: 338

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

AntiArt↑, 1,   AntiBio↑, 2,   diuretic↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 6,   Catalase↑, 4,   GPx↑, 2,   GSH↑, 2,   GSTs↑, 1,   HO-1↑, 1,   lipid-P↓, 1,   MDA↓, 2,   MDA↑, 1,   NRF2↓, 1,   NRF2↑, 4,   ROS↓, 10,   SOD↑, 4,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

AMPK↑, 1,   LDL↓, 1,   PKM2↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↑, 1,   MAPK↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

other↝, 3,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

ERK↓, 1,   GSK‐3β↓, 1,   HDAC↓, 1,   mTOR↓, 1,   PI3K↓, 1,  

Migration(tgid=13) ⓘ

PKCδ↑, 1,   TGF-β↓, 5,   VCAM-1↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

Hif1a↓, 2,   NO↓, 1,   NO↑, 1,  

Barriers & Transport(tgid=15) ⓘ

BBB↑, 2,   GastroP↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX1↓, 1,   COX2↓, 2,   ICAM-1↓, 1,   IL10↑, 1,   IL1β↓, 2,   IL4↓, 1,   IL6↓, 4,   Imm↑, 1,   Inflam↓, 8,   MUC2↓, 1,   NF-kB↓, 3,   PGE2↓, 1,   TNF-α↓, 2,  

Synaptic & Neurotransmission(tgid=18) ⓘ

tau↓, 1,   p‑tau↓, 1,  

Protein Aggregation(tgid=19) ⓘ

AGEs↓, 1,   Aβ↓, 1,   NLRP3↓, 2,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 2,   BioAv↑, 5,   eff↑, 2,  

Clinical Biomarkers(tgid=22) ⓘ

GutMicro↑, 4,   IL6↓, 4,   MUC19↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 3,   AntiDiabetic↑, 1,   AntiTum↑, 1,   cardioP↑, 3,   chemoP↑, 1,   cognitive↑, 2,   hepatoP↑, 4,   memory↑, 2,   neuroP↑, 5,   Obesity↓, 1,   radioP↑, 1,   toxicity↓, 3,   toxicity↝, 1,   toxicity∅, 3,   Wound Healing↑, 1,  

Infection & Microbiome(tgid=24) ⓘ

AntiFungal↑, 1,   AntiViral↑, 2,   Bacteria↓, 3,  

Ingredients & Constituents(tgid=25) ⓘ

CA↑, 1,   Catechins↑, 1,   FA↑, 1,   GA↑, 1,   Phen↑, 1,   QC↑, 1,  
Total Targets: 83

Scientific Paper Hit Count for: TGF-β, transforming growth factor-beta
10 Curcumin
6 Thymoquinone
5 Quercetin
4 Artemisinin
4 Ellagic acid
3 Apigenin (mainly Parsley)
3 Baicalein
3 Radiotherapy/Radiation
3 EGCG (Epigallocatechin Gallate)
3 Emodin
3 Garcinol
3 Resveratrol
3 Silymarin (Milk Thistle) silibinin
2 Allicin (mainly Garlic)
2 Ashwagandha(Withaferin A)
2 Berberine
2 Piperine
2 HydroxyTyrosol
2 Magnetic Fields
2 Propolis -bee glue
2 Shikonin
1 1,8-Cineole
1 3-bromopyruvate
1 Alpha-Lipoic-Acid
1 Andrographis
1 Betulinic acid
1 Caffeine
1 Celecoxib
1 Copper and Cu NanoParticles
1 Oxaliplatin
1 Date Fruit Extract
1 Gemcitabine (Gemzar)
1 Docetaxel
1 Eurycomanone
1 Fisetin
1 Shilajit/Fulvic Acid
1 Cisplatin
1 Paclitaxel
1 Ginkgo biloba
1 Gossypol
1 Hydroxycinnamic-acid
1 Lactoferrin
1 methotrexate
1 Luteolin
1 Bortezomib
1 Magnolol
1 MCToil
1 Metformin
1 Magnetic Field Rotating
1 Naringin
1 Rosmarinic acid
1 Selenium
1 Salvia miltiorrhiza
1 doxorubicin
1 Ursolic acid
1 Vitamin B5,Pantothenic Acid
1 Vitamin K2
Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:%  Target#:304  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

 

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