TumCI Cancer Research Results

TumCI, Tumor Cell invasion: Click to Expand ⟱
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Tumor cell invasion is a critical process in cancer progression and metastasis, where cancer cells spread from the primary tumor to surrounding tissues and distant organs. This process involves several key steps and mechanisms:

1.Epithelial-Mesenchymal Transition (EMT): Many tumors originate from epithelial cells, which are typically organized in layers. During EMT, these cells lose their epithelial characteristics (such as cell-cell adhesion) and gain mesenchymal traits (such as increased motility). This transition is crucial for invasion.

2.Degradation of Extracellular Matrix (ECM): Tumor cells secrete enzymes, such as matrix metalloproteinases (MMPs), that degrade the ECM, allowing cancer cells to invade surrounding tissues. This degradation facilitates the movement of cancer cells through the tissue.

3.Cell Migration: Once the ECM is degraded, cancer cells can migrate. They often use various mechanisms, including amoeboid movement and mesenchymal migration, to move through the tissue. This migration is influenced by various signaling pathways and the tumor microenvironment.

4.Angiogenesis: As tumors grow, they require a blood supply to provide nutrients and oxygen. Tumor cells can stimulate the formation of new blood vessels (angiogenesis) through the release of growth factors like vascular endothelial growth factor (VEGF). This not only supports tumor growth but also provides a route for cancer cells to enter the bloodstream.

5.Invasion into Blood Vessels (Intravasation): Cancer cells can invade nearby blood vessels, allowing them to enter the circulatory system. This step is crucial for metastasis, as it enables cancer cells to travel to distant sites in the body.

6.Survival in Circulation: Once in the bloodstream, cancer cells must survive the immune response and the shear stress of blood flow. They can form clusters with platelets or other cells to evade detection.

7.Extravasation and Colonization: After traveling through the bloodstream, cancer cells can exit the circulation (extravasation) and invade new tissues. They may then establish secondary tumors (metastases) in distant organs.

8.Tumor Microenvironment: The surrounding microenvironment plays a significant role in tumor invasion. Factors such as immune cells, fibroblasts, and signaling molecules can either promote or inhibit invasion and metastasis.
Scientific Papers found: Click to Expand⟱
5260- 3BP,    Systemic Delivery of Microencapsulated 3-Bromopyruvate for the Therapy of Pancreatic Cancer
- in-vivo, PC, NA
TumCG↓, In vivo, animals treated with β-CD–3-BrPA demonstrated minimal or no tumor progression as evident by the BLI signal
toxicity↓, In contrast to animals treated with free 3-BrPA, no lethal toxicity was observed for β-CD–3-BrPA.
BioAv↝, It is possible that in the microencapsulated formulation, 3-BrPA, is more bioavailable for uptake into tumor cells and less available to the normal cells that apparently mediate its toxicity
GAPDH↓, 3-Bromopyruvate (3-BrPA), a highly potent small-molecular inhibitor of the enzyme GAPDH, represents the only available antiglycolytic drug candidate that is able to enter cancer cells selectively through the monocarboxylate transporter 1 (MCT1; refs.
toxicity↑, However, due to its alkylating properties, 3-BrPA is associated with significant toxicity when delivered systemically in therapeutic doses, which has impeded the clinical development and use of this drug in patients with cancer
Dose↝, Encapsulation of 3-BrPA in β-CD was achieved by portionwise addition of 3-BrPA (166 mg, 1 mmol/L) to a stirring solution of β-CD (1,836 mg in 30 mL DI water). The resulting solution was sonicated for 1 hour at room temperature and then shaken overnig
ATP↓, ability of microencapsulated 3-BrPA (β-CD-3-BrPA) to achieve dose-dependent ATP depletion and cell death, two human pancreatic cancer cell lines were employed.
eff↑, both PDAC cell lines were more sensitive to the drugs when hypoxic (Fig. 2)
TumCI↓, MiaPaCa-2 and Suit-2 cells showed a reduction in invasion at drug concentrations as low as 12.5 µmol/L.
MMP9↓, marked reduction in the secretion of MMP-9 was detected in both cell lines.
toxicity↓, No organ toxicities or tissue damage was observed in animals treated with β-CD–3-BrPA

1333- AG,    Astragalus polysaccharide inhibits breast cancer cell migration and invasion by regulating epithelial-mesenchymal transition via the Wnt/β-catenin signaling pathway
- in-vitro, BC, NA
TumCMig↓,
TumCI↓,
Ki-67↓,
TumCP↓,
Snail↓,
Vim↓,
E-cadherin↑,
Wnt↓,
β-catenin/ZEB1↓,

1338- AG,    The Modulatory Properties of Astragalus membranaceus Treatment on Triple-Negative Breast Cancer: An Integrated Pharmacological Method
- in-vitro, BC, NA
TumCI↓,
Apoptosis↑,
Symptoms↓,
PIK3CA↓,
Akt↓,
Bcl-2↓,

5431- AG,    Advances in research on the anti-tumor mechanism of Astragalus polysaccharides
- Review, Var, NA
AntiTum↑, APS has been increasingly used in cancer therapy owing to its anti-tumor ability as it prevents the progression of prostate, liver, cervical, ovarian, and non-small-cell lung cancer by suppressing tumor cell growth and invasion and enhancing apoptosi
TumCG↓,
TumCI↓,
Apoptosis↑, after APS treatment, the apoptosis of HepG2 cells is accelerated (57).
Imm↑, APS enhances the sensitivity of tumors to antineoplastic agents and improves the body’s immunity
Bcl-2↓, Huang et al. proposed that APS induces H22 (a hepatocellular cancer [HCC] cell line) apoptosis by downregulating Bcl-2 and upregulating Bax expression (56).
BAX↑,
Wnt↓, downregulating the Wnt/β-catenin signaling pathway.
β-catenin/ZEB1↓,
TumCG↓, APS effectively inhibited the growth of MDA-MB-231 (a human breast cancer [BC] cell line) graft tumor (58)
miR-133a-3p↑, apoptosis rate of human osteosarcoma MG63 cells increased owing to the upregulation of miR-133a and inactivation of the JNK signaling pathways (71).
JNK↓,
Fas↑, Li and Shen found that APS can induce apoptosis by activating the Fas death receptor pathway.
P53↑, Zhang et al. showed that APS could activate p53 and p21 and inhibit the expression of Notch1 and Notch3 in vitro, ultimately inhibiting cell proliferation and promoting their apoptosis
P21↑,
NOTCH1↓,
NOTCH3↓,
TumCP↓,
TumCCA↑, Liu et al. found that APS induced the cell cycle of bladder cancer UM-UC-3 to stop in the G0/G1 phase, thus inhibiting its proliferation
GPx4↓, APS was found to reduce GPX4 expression, inhibit the activity of the light chain subunit SLC7A11 (xCT), and promote the formation of BECN1-xCT complex by activating AMPK/BECN1 signaling.
xCT↓,
AMPK↑,
Beclin-1↑,
NF-kB↓, APS could control the proliferation of lung cancer cells (A549 and NCI-H358 cells) by inhibiting the NF-κB signaling pathway (97)
EMT↓, APS treatment led to reduced EMT markers (vimentin, AXL) and MIF levels in cells.
Vim↓,
TumMeta↓, APS inhibits Lewis lung cancer growth and metastasis in mice by significantly reducing VEGF and EGFR expression in cancerous tissues
VEGF↓,
EGFR↓,
eff↑, Nano-drug delivery systems can increase efficiency and reduce toxicity
eff↑, Jiao et al. developed selenium nanoparticles modified with macromolecular weight APS and observed positive results in hepatoma treatment
MMP↓, Subsequent investigations revealed that APS can decrease the ΔΨm values and Bcl-2, p-PI3K, P-gp, and p-AKT levels while elevating Bax expression.
P-gp↓,
MMP9↓, downregulation of MMP-9 expression,
ChemoSen↑, Li et al. observed that APS could enhance the sensitivity of SKOV3 ovarian cancer cells to CDDP treatment by activating the mitochondrial apoptosis pathway and JNK1/2 signaling pathway
SIRT1↓, APS significantly suppressed SIRT1 and SREBP1 expression, decreased cholesterol and triglyceride levels in PC3 and DU145, and attenuated cell proliferation.
SREBP1↓,
TumAuto↑, APS can induce autophagy in colorectal cancer cells by inhibiting the PI3K/AKT/mTOR axis and the development of cancer cells.
PI3K↓,
mTOR↓,
Casp3↑, Shen found that APS elevated caspase-9, caspase-3, and Bax protein levels, decreased Bcl-2 protein expression, and inhibited CD133 and CD44 co-positive colon cancer stem cell proliferation time
Casp9↑,
CD133↓,
CD44↓,
CSCs↓,
QoL↑, QOL was significantly improved as indicated by the reduction in pain and improvement in appetite

5433- AG,    Mechanisms of astragalus polysaccharide enhancing STM2457 therapeutic efficacy in m6A-mediated OSCC treatment
- vitro+vivo, OS, NA
other↓, Combined STM2457 and APS treatment significantly reduced m6A levels, METTL3, HNRNPA2B1, and FOXQ1 expression, and mRNA stability compared to single-drug treatments, approaching or surpassing METTL3 silencing effects.
TumCP↓, The combination markedly suppressed cell proliferation, migration, invasion, and EMT, with increased E-cadherin and decreased N-cadherin levels.
TumCMig↓,
TumCI↓,
EMT↓,
E-cadherin↑,
N-cadherin↓,
TumCG↓, In vivo, combination therapy significantly reduced tumor growth and FOXQ1 expression, outperforming single-drug treatments.

5438- AG,    Mechanisms of astragalus polysaccharide enhancing STM2457 therapeutic efficacy in mA-mediated OSCC treatment
- vitro+vivo, NA, NA
TumCP↓, combination markedly suppressed cell proliferation, migration, invasion, and EMT, with increased E-cadherin and decreased N-cadherin levels.
TumCMig↓,
TumCI↓,
EMT↓,
E-cadherin↑,
N-cadherin↓,

4426- AgNPs,    Antiangiogenic properties of silver nanoparticles
- Study, NA, NA
angioG↑, Ag-NPs might have the ability to inhibit angiogenesis, the pivotal step in tumor growth, invasiveness, and metastasis.
TumCG↓,
TumCI↓,
TumMeta↓,
VEGF↓, demonstrated that Ag-NPs could also inhibit vascular endothelial growth factor (VEGF) induced cell proliferation, migration, and capillary-like tube formation of bovine retinal endothelial cells like PEDF.
PI3K↓, inhibition of the PI3K/Akt cell-survival signal in a similar pattern of PEDF.
Akt↓,

5147- AgNPs,    Size dependent anti-invasiveness of silver nanoparticles in lung cancer cells
- in-vitro, Lung, A549
TumCMig↓, 13 nm AgNPs significantly inhibit the migration and invasiveness of lung adenocarcinoma A549 cells, induce elevated reactive oxygen species and lead to NF-κB directed cellular apoptosis
TumCI↓,
ROS↑,
p‑NF-kB↑, 13 nm AgNPs was able to significantly upregulate the phosphorylation of NF-κB (p-NF-κB) in A549 cells
selectivity↑, we speculate that, AgNPs, which are pointed out that have a sustained release of Ag+ in an environment with lower pH (such as cancer cells)
eff↝, and this inhibitive effect is most pronounced treated with 13 nm AgNPs, while the effect starts decreasing with the size of 45 nm and completely vanishes for 92 nm AgNPs.

359- AgNPs,    Anti-cancer & anti-metastasis properties of bioorganic-capped silver nanoparticles fabricated from Juniperus chinensis extract against lung cancer cells
- in-vitro, Lung, A549 - in-vitro, Nor, HEK293
Casp3↑,
Casp9↑,
P53↑,
ROS↑,
MMP2↓,
MMP9↓,
TumCCA↑, cessation in the G0/G1 phase
*toxicity↓, 9.87ug/ml(cancer cells) and 111.26 µg/ml(normal cells)
TumCMig↓,
TumCI↓,

5343- Ajoene,    The garlic compound ajoene covalently binds vimentin, disrupts the vimentin network and exerts anti-metastatic activity in cancer cells
- in-vitro, Cerv, HeLa - in-vitro, BC, MDA-MB-231
Vim↑, Surprisingly, and apparently contradictory to the role that vimentin plays in metastasis, a time-dependent increase in total vimentin protein was observed
TumCI↓, Ajoene inhibits invasion and migration
TumCMig↓,
TumMeta↓, offer protection against metastatic cancer, mediated through binding to the vimentin target.
Vim↓, our vimentin finding is therefore the second example in the literature, where ajoene has been found to target and inhibit a protein, with a simultaneous increase in its expression.
other↝, We argue that ajoenes increased vimentin expression may be a response to restore the malfunctioning vimentin network.

3442- ALA,    α‑lipoic acid modulates prostate cancer cell growth and bone cell differentiation
- in-vitro, Pca, 22Rv1 - in-vitro, Pca, C4-2B - in-vitro, Nor, 3T3
tumCV↓, Notably, α‑LA treatment significantly reduced the cell viability, migration, and invasion of PCa cell lines in a dose‑dependent manner.
TumCMig↓,
TumCI↓,
ROS↑, α‑LA supplementation dramatically increased reactive oxygen species (ROS) levels and HIF‑1α expression, which started the downstream molecular cascade and activated JNK/caspase‑3 signaling pathway
Hif1a↑, The expression of HIF-1α significantly increased following α-LA treatment and was comparable with the changes in ROS.
JNK↑,
Casp↑,
TumCCA↑, arrest of the cell cycle in the S‑phase, which has led to apoptosis of PCa cells
Apoptosis↑,
selectivity↑, Also, the treatment of α‑LA improved bone health by reducing PCa‑mediated bone cell modulation.

297- ALA,    Insights on the Use of α-Lipoic Acid for Therapeutic Purposes
- Review, BC, SkBr3 - Review, neuroblastoma, SK-N-SH - Review, AD, NA
PDH↑, ALA is capable of activating pyruvate dehydrogenase in tumor cells.
TumCG↓, ALA also significantly inhibited tumor growth in mouse xenograft model using BCPAP and FTC-133 cells
ROS↑, ALA is able to generate ROS, which promote ALA-dependent cell death in lung cancer [75], breast cancer [76] and colon cancer
AMPK↑,
EGR4↓,
Half-Life↓, Data suggests that ALA has a short half-life and bioavailability (about 30%)
BioAv↝,
*GSH↑, Moreover, it is able to increase the glutathione levels inside the cells, that chelate and excrete a wide variety of toxins, especially toxic metals from the body
*IronCh↑, The existence of thiol groups in ALA is responsible for its metal chelating abilities [14,35].
*ROS↓, ALA exerts a direct impact in oxidative stress reduction
*antiOx↑, ALA is being referred as the universal antioxidant
*neuroP↑, ALA has neuroprotective effects on Aβ-mediated cytotoxicity
*Ach↑, ALA show anti-dementia or anti-AD properties by increasing acetylcholine (ACh) production through activation of choline acetyltransferase, which increases glucose absorption
*lipid-P↓, ALA has multiple and complex effects in this way, namely scavenging ROS, transition metal ions, increasing the levels of reduced glutathione [59,63], scavenging of lipid peroxidation products
*IL1β↓, ALA downregulated the levels of the inflammatory cytokines IL-1B and IL-6 in SK-N-BE human neuroblastoma cells
*IL6↓,
TumCP↓, ALA inhibited cell proliferation, [18F]-FDG uptake and lactate formation and increased apoptosis in neuroblastoma cell lines Kelly, SK-N-SH, Neuro-2a and in the breast cancer cell line SkBr3.
FDG↓,
Apoptosis↑,
AMPK↑, ALA suppressed thyroid cancer cell proliferation and growth through activation of AMPK and subsequent down-regulation of mTOR-S6 signaling pathway in BCPAP, HTH-83, CAL-62 and FTC-133 cells lines.
mTOR↓,
EGFR↓, ALA inhibited cell proliferation through Grb2-mediated EGFR down-regulation
TumCI↓, ALA inhibited metastatic breast cancer cells migration and invasion, partly through ERK1/2 and AKT signaling
TumCMig↓,
*memory↑, Alzheimer’s Disease: ALA led to a marked improvement in learning and memory retention
*BioAv↑, Since ALA is poorly soluble, lecithin has been used as an amphiphilic matrix to enhance its bioavailability.
*BioAv↝, ALA were found to be considerably higher in adults with mean age greater than 75 years as compared to young adults between the ages of 18 and 45 years.
*other↓, ALA treatment has been recently studied by some clinical trials to explain its efficacy in preventing miscarriage
*other↝, 1800 mg of ALA or placebo were administrated orally every day, except during the period 2 days before to 4 days after administration of each dose of platinum to avoid potential interference with platinum’s antitumor effects
*Half-Life↓, Data shows a short half-life and bioavailability of about 30% of ALA due to mechanisms involving hepatic degradation, reduced ALA solubility as well as instability in the stomach.
*BioAv↑, ALA bioavailability is greatly reduced after food intake and it has been recommended that ALA should be admitted at least 2 h after eating or if taken before; meal should be taken at least 30 min after ALA administration
*ChAT↑, ALA show anti-dementia or anti-AD properties by increasing acetylcholine (ACh) production through activation of choline acetyltransferase, which increases glucose absorption
*GlucoseCon↑,

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

1252- aLinA,    α-Linolenic acid induces apoptosis, inhibits the invasion and metastasis, and arrests cell cycle in human breast cancer cells by inhibiting fatty acid synthase
- in-vitro, BC, NA
FASN↓, α-linolenic acid (ALA) as a novel fatty acid synthase (FASN) inhibitor
Apoptosis↑,
TumCI↓,
TumMeta↓,
TumCCA↑,

1157- And,    Andrographolide suppresses the migratory ability of human glioblastoma multiforme cells by targeting ERK1/2-mediated matrix metalloproteinase-2 expression
- in-vitro, GBM, GBM8401 - in-vitro, GBM, U251
TumCI↓,
TumCMig↓,
MMP2↓,
ERK↝, combination of andrographolide and an ERK inhibitor might be a good strategy for preventing GBM metastasis

1548- Api,    A comprehensive view on the apigenin impact on colorectal cancer: Focusing on cellular and molecular mechanisms
- Review, Colon, NA
*BioAv↓, Apigenin is not easily absorbed orally because of its low water solubility, which is only 2.16 g/mL
*Half-Life∅, Apigenin is slowly absorbed and eliminated from the body, as evidenced by its half‐life of 91.8 h in the blood
selectivity↑, selective anticancer effects and effective cell cytotoxic activity while exhibiting negligible toxicity to ordinary cells
*toxicity↓, intentional consumption in higher doses, as the toxicity hazard is low
Wnt/(β-catenin)↓, inhibiting the Wnt/β‐catenin
P53↑,
P21↑,
PI3K↓,
Akt↓,
mTOR↓,
TumCCA↑, G2/M
TumCI↓,
TumCMig↓,
STAT3↓, apigenin can activate p53, which improves catalase and inhibits STAT3,
PKM2↓,
EMT↓, reversing increases in epithelial–mesenchymal transition (EMT)
cl‑PARP↑, apigenin increases the cleavage of poly‐(ADP‐ribose) polymerase (PARP) and rapidly enhances caspase‐3 activity,
Casp3↑,
Bax:Bcl2↑,
VEGF↓, apigenin suppresses VEGF transcription
Hif1a↓, decrease in hypoxia‐inducible factor 1‐alpha (HIF‐1α
Dose∅, effectiveness of apigenin (200 and 300 mg/kg) in treating CC was evaluated by establishing xenografts on Balb/c nude mice.
GLUT1↓, Apigenin has been found to inhibit GLUT1 activity and glucose uptake in human pancreatic cancer cells
GlucoseCon↓,

1565- Api,    Apigenin-7-glucoside induces apoptosis and ROS accumulation in lung cancer cells, and inhibits PI3K/Akt/mTOR pathway
- in-vitro, Lung, A549 - in-vitro, Nor, BEAS-2B - in-vitro, Lung, H1975
TumCP↓, AGL significantly reduced proliferation, promoted cell apoptosis, and attenuated the migration and invasion of A549 or H1975 cell
Apoptosis↑,
TumCMig↓,
TumCI↓,
Cyt‑c↑, elevated the levels of cytochrome C and MDA
MDA↑,
GSH↓, but reduced the production of GSH in A549 and H1975 cells.
ROS↑, AGL enhanced the accumulation of ROS
PI3K↓, induces ROS accumulation in lung cancer cells by repressing PI3K/Akt/mTOR pathway
Akt↓,
mTOR↓,

1545- Api,    The Potential Role of Apigenin in Cancer Prevention and Treatment
- Review, NA, NA
TNF-α↓, Apigenin downregulates the TNFα
IL6↓,
IL1α↓,
P53↑,
Bcl-xL↓,
Bcl-2↓,
BAX↑,
Hif1a↓, Apigenin inhibited HIF-1alpha and vascular endothelial growth factor expression
VEGF↓,
TumCCA↑, Apigenin exposure induces G2/M phase cell cycle arrest, DNA damage, apoptosis and p53 accumulation
DNAdam↑,
Apoptosis↑,
CycB/CCNB1↓,
cycA1/CCNA1↓,
CDK1↓,
PI3K↓,
Akt↓,
mTOR↓,
IKKα↓, , decreases IKKα kinase activity,
ERK↓,
p‑Akt↓,
p‑P70S6K↓,
p‑S6↓,
p‑ERK↓, decreased the expression of phosphorylated (p)-ERK1/2 proteins, p-AKT and p-mTOR
p‑P90RSK↑,
STAT3↓,
MMP2↓, Apigenin down-regulated Signal transducer and activator of transcription 3target genes MMP-2, MMP-9 and vascular endothelial growth factor
MMP9↓,
TumCP↓, Apigenin significantly suppressed colorectal cancer cell proliferation, migration, invasion and organoid growth through inhibiting the Wnt/β-catenin signaling
TumCMig↓,
TumCI↓,
Wnt/(β-catenin)↓,

2632- Api,    Apigenin inhibits migration and induces apoptosis of human endometrial carcinoma Ishikawa cells via PI3K-AKT-GSK-3β pathway and endoplasmic reticulum stress
- in-vitro, EC, NA
TumCP↓, We found that API could inhibit the proliferation of Ishikawa cells at IC50 of 45.55 μM, arrest the cell cycle at G2/M phase, induce apoptosis by inhibiting Bcl-xl and increasing Bax, Bak and Caspases.
TumCCA↑,
Apoptosis↑,
Bcl-2↓,
BAX↑,
Bak↑,
Casp↑,
ER Stress↑, Further, API could induce apoptosis by activating the endoplasmic reticulum (ER) stress pathway by increasing the Ca2+, ATF4, and CHOP.
Ca+2↑, after API treatment for 48 h, the intracellular Ca2+ concentration increased in cells in a dose-dependent manner.
ATF4↑,
CHOP↑,
ROS↑, the level of intracellular ROS increased gradually with the increase of API concentration.
MMP↓, mitochondrial membrane potential of 30 μM, 50 μM, and 70 μM groups decreased by 2.19%, 11.32%, and 14.91%, respectively.
TumCMig↓, API inhibits the migration and invasion of Ishikawa cells and the migration and invasion related gene and protein.
TumCI↓,
eff↑, In our study, API restrained the viability of Ishikawa cells, and the inhibition effect of API on Ishikawa cells was better than that of 5-FU.
P53↑, API induces p53 tumor suppressor proteins at the translational level and the induces p21
P21↑,
Cyt‑c↑, After the mitochondria release the Cyto-c, the Caspase-9 is activated, resulting in increased activity of Caspases
Casp9↑, In our study, the expression levels of Bad, Bax, Cyto-c, Caspase-9 and Caspase-3 proteins were up-regulated,
Casp3↑,
Bcl-xL↓, while the expression level of Bcl-xl was down-regulated

2640- Api,    Apigenin: A Promising Molecule for Cancer Prevention
- Review, Var, NA
chemoPv↑, considerable potential for apigenin to be developed as a cancer chemopreventive agent.
ITGB4↓, apigenin inhibits hepatocyte growth factor-induced MDA-MB-231 cells invasiveness and metastasis by blocking Akt, ERK, and JNK phosphorylation and also inhibits clustering of β-4-integrin function at actin rich adhesive site
TumCI↓,
TumMeta↓,
Akt↓,
ERK↓,
p‑JNK↓,
*Inflam↓, The anti-inflammatory properties of apigenin are evident in studies that have shown suppression of LPS-induced cyclooxygenase-2 and nitric oxide synthase-2 activity and expression in mouse macrophages
*PKCδ↓, Apigenin has been reported to inhibit protein kinase C activity, mitogen activated protein kinase (MAPK), transformation of C3HI mouse embryonic fibroblasts and the downstream oncogenes in v-Ha-ras-transformed NIH3T3 cells (43, 44).
*MAPK↓,
EGFR↓, Apigenin treatment has been shown to decrease the levels of phosphorylated EGFR tyrosine kinase and of other MAPK and their nuclear substrate c-myc, which causes apoptosis in anaplastic thyroid cancer cells
CK2↓, apigenin has been shown to inhibit the expression of casein kinase (CK)-2 in both human prostate and breast cancer cells
TumCCA↑, apigenin induces a reversible G2/M and G0/G1 arrest by inhibiting p34 (cdc2) kinase activity, accompanied by increased p53 protein stability
CDK1↓, inhibiting p34 (cdc2) kinase activity
P53↓,
P21↑, Apigenin has also been shown to induce WAF1/p21 levels resulting in cell cycle arrest and apoptosis in androgen-responsive human prostate cancer
Bax:Bcl2↑, Apigenin treatment has been shown to alter the Bax/Bcl-2 ratio in favor of apoptosis, associated with release of cytochrome c and induction of Apaf-1, which leads to caspase activation and PARP-cleavage
Cyt‑c↑,
APAF1↑,
Casp↑,
cl‑PARP↑,
VEGF↓, xposure of endothelial cells to apigenin results in suppression of the expression of VEGF, an important factor in angiogenesis via degradation of HIF-1α protein
Hif1a↓,
IGF-1↓, oral administration of apigenin suppresses the levels of IGF-I in prostate tumor xenografts and increases levels of IGFBP-3, a binding protein that sequesters IGF-I in vascular circulation
IGFBP3↑,
E-cadherin↑, apigenin exposure to human prostate carcinoma DU145 cells caused increase in protein levels of E-cadherin and inhibited nuclear translocation of β-catenin and its retention to the cytoplasm
β-catenin/ZEB1↓,
HSPs↓, targets of apigenin include heat shock proteins (61), telomerase (68), fatty acid synthase (69), matrix metalloproteinases (70), and aryl hydrocarbon receptor activity (71) HER2/neu (72), casein kinase 2 alpha
Telomerase↓,
FASN↓,
MMPs↓,
HER2/EBBR2↓,
CK2↓,
eff↑, The combination of sulforaphane and apigenin resulted in a synergistic induction of UGT1A1
AntiAg↑, Apigenin inhibit platelet function through several mechanisms including blockade of TxA
eff↑, ex vivo anti-platelet effect of aspirin in the presence of apigenin, which encourages the idea of the combined use of aspirin and apigenin in patients in which aspirin fails to properly suppress the TxA
FAK↓, Apigenin inhibits expression of focal adhesion kinase (FAK), migration and invasion of human ovarian cancer A2780 cells.
ROS↑, Apigenin generates reactive oxygen species, causes loss of mitochondrial Bcl-2 expression, increases mitochondrial permeability, causes cytochrome C release, and induces cleavage of caspase 3, 7, 8, and 9 and the concomitant cleavage of the inhibitor
Bcl-2↓,
Cyt‑c↑,
cl‑Casp3↑,
cl‑Casp7↑,
cl‑Casp8↑,
cl‑Casp9↑,
cl‑IAP2↑,
AR↓, significant decrease in AR protein expression along with a decrease in intracellular and secreted forms of PSA. Apigenin treatment of LNCaP cells
PSA↓,
p‑pRB↓, apigenin inhibited hyperphosphorylation of the pRb protein
p‑GSK‐3β↓, Inhibition of p-Akt by apigenin resulted in decreased phosphorylation of GSK-3beta.
CDK4↓, both flavonoids exhibited cell growth inhibitory effects which were due to cell cycle arrest and downregulation of the expression of CDK4
ChemoSen↑, Combination therapy of gemcitabine and apigenin enhanced anti-tumor efficacy in pancreatic cancer cells (MiaPaca-2, AsPC-1)
Ca+2↑, apigenin in neuroblastoma SH-SY5Y cells resulted in increased apoptosis, which was associated with increases in intracellular free [Ca(2+)] and Bax:Bcl-2 ratio, mitochondrial release of cytochrome c and activation of caspase-9, calpain, caspase-3,12
cal2↑,

2641- Api,    Apigenin inhibits HGF-promoted invasive growth and metastasis involving blocking PI3K/Akt pathway and beta 4 integrin function in MDA-MB-231 breast cancer cells
- in-vitro, BC, MDA-MB-231
TumCMig↓, apigenin presents the most potent anti-migration and anti-invasion properties
TumCI↓,
ITGB4↓, Apigenin inhibits the HGF-induced clustering of beta 4 integrin at actin-rich adhesive site and lamellipodia through PI3K-dependent manner.

2593- Api,    Apigenin promotes apoptosis of 4T1 cells through PI3K/AKT/Nrf2 pathway and improves tumor immune microenvironment in vivo
- in-vivo, BC, 4T1
TumCP↓, API suppresses 4T1 cells proliferation
TumCMig↓, API restraints 4T1 cells migration and invasion
TumCI↓,
Apoptosis↑, API triggers 4T1 apoptosis and modulates the expression levels of apoptotic-associated proteins in 4T1 cells
MMP↑, API triggers the depolarization of ΔΨm in 4T1 cells
ROS↑, API induces ROS generation
p‑PI3K↓, The results revealed a significant downregulation of p-PI3K/PI3K, p-AKT/AKT, and Nrf2 in 4T1 cells following API treatment
PI3K↓,
Akt↓,
NRF2↓,
AntiTum↑, API exhibits anti-tumor activity in mice
OS↑, results of animal survival experiments show that API can appropriately prolong the survival of mice with mammary gland tumors

175- Api,    Apigenin up-regulates transgelin and inhibits invasion and migration of colorectal cancer through decreased phosphorylation of AKT
- vitro+vivo, CRC, SW480 - vitro+vivo, CRC, DLD1 - vitro+vivo, CRC, LS174T
MMP↓,
p‑Akt↓,
TumCP↓, Apigenin inhibits cell proliferation and invasion
TumCI↓,
NADH↓, down-regulated proteins by apigenin included NADH dehydrogenase [ubiquinone] iron-sulphur protein 3, heat shock protein HSP 90-alpha, stress-70 protein and NADH dehydrogenase
HSP90↓,
other↑, whereas the up-regulated proteins include Transgelin, Ras-related protein Rab-3D and 28S ribosomal protein S22
talin?,

172- Api,    Apigenin suppresses colorectal cancer cell proliferation, migration and invasion via inhibition of the Wnt/β-catenin signaling pathway
- in-vitro, CRC, SW480 - in-vitro, CRC, HTC15
Wnt/(β-catenin)↓, Apigenin inhibits β‑catenin/TCF/LEF signal activation.
TCF↓,
LEF1↓, LEF
TumCP↓, Apigenin inhibits CRC cell line proliferation
TumCMig↓, Apigenin inhibits migration and invasion of SW480 cells and growth of intestinal organoids.
TumCI↓,

174- Api,    Downregulation of NEDD9 by apigenin suppresses migration, invasion, and metastasis of colorectal cancer cells
- in-vitro, CRC, SW480 - in-vitro, CRC, DLD1
NEDD9↓, Inhibition of apigenin on cell migration, invasion, and metastasis through downregulation of NEDD9 in vitro and in vivo
TumCMig↓, Apigenin attenuates NEDD9 expression, resulting in inhibition on cell migration, invasion, and metastasis of those cells.
TumCI↓,

3396- ART/DHA,    Progress on the study of the anticancer effects of artesunate
- Review, Var, NA
TumCP↓, reported inhibitory effects on cancer cell proliferation, invasion and migration.
TumCI↓,
TumCMig↓,
Apoptosis↑, ART has been reported to induce apoptosis, differentiation and autophagy in colorectal cancer cells by impairing angiogenesis
Diff↑,
TumAuto↑,
angioG↓,
TumCCA↑, inducing cell cycle arrest (11), upregulating ROS levels, regulating signal transduction [for example, activating the AMPK-mTOR-Unc-51-like autophagy activating kinase (ULK1) pathway in human bladder cancer cells]
ROS↑,
AMPK↑,
mTOR↑,
ChemoSen↑, ART has been shown to restore the sensitivity of a number of cancer types to chemotherapeutic drugs by modulating various signaling pathways
Tf↑, ART could upregulate the mRNA levels of transferrin receptor (a positive regulator of ferroptosis), thus inducing apoptosis and ferroptosis in A549 non-small cell lung cancer (NSCLC) cells.
Ferroptosis↑,
Ferritin↓, ferritin degradation, lipid peroxidation and ferroptosis
lipid-P↑,
CDK1↑, Cyclin-dependent kinase 1, 2, 4 and 6
CDK2↑,
CDK4↑,
CDK6↑,
SIRT1↑, Sirt1 levels
COX2↓,
IL1β↓, IL-1? ?
survivin↓, ART can selectively downregulate the expression of survivin and induce the DNA damage response in glial cells to increase cell apoptosis and cell cycle arrest, resulting in increased sensitivity to radiotherapy
DNAdam↑,
RadioS↑,

574- ART/DHA,    Dihydroartemisinin suppresses glioma proliferation and invasion via inhibition of the ADAM17 pathway
TumCP↓,
TumCMig↓,
TumCI↓,
MMP17↓,
p‑EGFR↓,
p‑Akt↓,

570- ART/DHA,    Artemisinin and its derivatives can significantly inhibit lung tumorigenesis and tumor metastasis through Wnt/β-catenin signaling
- vitro+vivo, NSCLC, A549 - vitro+vivo, NSCLC, H1299
TumCCA↑, arresting cell cycle in G1 phase.
CSCs↓,
TumCI↓,
TumCMig↓,
TumCG↓,
Wnt/(β-catenin)↓, main pathway
Nanog↓,
SOX2↓,
OCT4↓, oct3/4
N-cadherin↓,
Vim↓,
E-cadherin↑,

1099- ART/DHA,    Dihydroartemisinin inhibits IL-6-induced epithelial–mesenchymal transition in laryngeal squamous cell carcinoma via the miR-130b-3p/STAT3/β-catenin signaling pathway
- in-vitro, NA, NA
EMT↓,
TumCI↓,
STAT3↓,
β-catenin/ZEB1↓,

5415- ASA,    The Anti-Metastatic Role of Aspirin in Cancer: A Systematic Review
- Review, Var, NA
TumMeta↓, The included studies demonstrated that aspirin suppresses metastatic dissemination across multiple cancer types through coordinated platelet-dependent and tumor-intrinsic mechanisms.
COX1↓, Aspirin consistently inhibited platelet aggregation and COX-1-dependent TXA2 production, disrupting platelet–tumor cell interactions, intravascular metastatic niche formation, and platelet-mediated immune suppression.
TXA2↓,
AntiAg↑, Beyond platelet effects, aspirin suppressed EMT, migration, and invasion through modulation of EMT transcriptional regulators and inflammatory signaling pathways.
EMT↓,
TumCMig↓,
TumCI↓,
AMPK↑, Additional mechanisms included activation of AMPK, inhibition of c-MYC signaling, regulation of redox-responsive pathways and impairment of anoikis resistance.
cMyc↓,
PGE2↓, Importantly, oral aspirin (20 mg/kg/day; human-equivalent ≈ 150 mg/day), administered before tumor cell injection, prevented platelet-induced metastatic enhancement and suppressed TXA2 and PGE2 production.
Dose↑, medium and high doses of aspirin reduced pulmonary metastatic burden by more than 50%, whereas low-dose aspirin was ineffective.
RadioS↑, Wang et al. [45] demonstrated that low-dose aspirin suppresses radiotherapy-induced release of immunosuppressive exosomes in breast cancer, restoring NK-cell proliferation and enhancing antitumor immunity in vivo.
PD-L1↓, Similarly, Xiao et al. [46] showed that aspirin epigenetically downregulates PD-L1 expression by inhibiting KAT5-dependent histone acetylation, thereby restoring T-cell activation
E-cadherin↑, Aspirin restored E-cadherin expression and suppressed EMT regulators, including Slug, vimentin, Twist, MMP-2, and MMP-9.
EMT↓,
Slug↓,
Vim↓,
Twist↓,
MMP2↓,
MMP9↓,
other↑, definitive conclusions regarding clinical efficacy across cancer types cannot yet be drawn. Nevertheless, the consistency of mechanistic signals across experimental systems supports further investigation of aspirin as a low-cost adjunct in oncology

5398- Ash,    Withaferin-A inhibits colorectal cancer growth and metastasis by targeting the HSP90/HIF-1α/EMT axis
- in-vitro, CRC, HCT116 - in-vitro, CRC, SW48
TumCG↓, WA inhibits CRC’s growth, migration, and invasion by inhibiting the HSP90/HIF-1α/EMT axis.
TumCMig↓,
TumCI↓,
HSP90↓,
Hif1a↓,
EMT↓,

3174- Ash,    Withaferin A Acts as a Novel Regulator of Liver X Receptor-α in HCC
- in-vitro, HCC, HepG2 - in-vitro, HCC, Hep3B - in-vitro, HCC, HUH7
NF-kB↓, We found that many of Nuclear factor kappa B (NF-κB), angiogenesis and inflammation associated proteins secretion is downregulated upon Withaferin A treatment.
angioG↓,
Inflam↓,
TumCP↓, uppressed the proliferation, migration, invasion, and anchorage-independent growth of these HCC cells.
TumCMig↓,
TumCI↓,
Sp1/3/4↓, Withaferin A inhibits NF-κB, Specificity protein 1 (Sp1) transcription factors, and downregulates Vascular Endothelial Growth Factor (VEGF) gene expression
VEGF↓,
angioG↓, Withaferin A (2.5 µM) treatment decreased the secretion of various angiogenesis-related markers, growth factors, and cytokines (Serpin F1(PEDF), uPA, PDGF-AA, Angiogenin, Endothelin-1, Macrophage migration inhibitory factor (MIF), PAI-1, MCP1, ICAM-1
uPA↓,
PDGF↓,
MCP1↓,
ICAM-1↓,
*NRF2↑, It also upregulates the Nuclear factor erythroid 2-related factor 2 (Nrf2) transcription factor and protects from Acetaminophen-induced hepatotoxicity and liver injury
*hepatoP↑,

3172- Ash,    Implications of Withaferin A for the metastatic potential and drug resistance in hepatocellular carcinoma cells via Nrf2-mediated EMT and ferroptosis
- in-vitro, HCC, HepG2 - in-vitro, Nor, HL7702
Keap1↑, Notably, Withaferin A elevated Keap1 expression to mitigate Nrf2 signaling activation-mediated epithelial to mesenchymal transition (EMT) and ferroptosis-related protein xCT expression
NRF2↓,
EMT↓, Withaferin A suppresses epithelial-to-mesenchymal transition (EMT) in non-small cell lung cancer
TumCP↓, Withaferin A restrains proliferation, invasion, and VM of hepatoma cells while preserving normal hepatocytes
TumCI↓,
selectivity↑, , treatment with Withaferin A ranging from 1 to 100 μM had little effect on cell viability of human normal liver cells (HL-7702 cells), indicating the little cytotoxicity on normal hepatocytes.
*toxicity↓,
ROS↑, Withaferin A strikingly enhanced ROS () and MDA levels (), but reduced the GSH levels (), indicating the induction of ferroptosis by Withaferin A
MDA↑,
GSH↓,
Ferroptosis↑,

1358- Ash,    Withaferin A: A Dietary Supplement with Promising Potential as an Anti-Tumor Therapeutic for Cancer Treatment - Pharmacology and Mechanisms
- Review, Var, NA
TumCCA↑,
Apoptosis↑,
TumAuto↑,
Ferroptosis↑,
TumCP↓,
CSCs↓,
TumMeta↓,
EMT↓,
angioG↓,
Vim↓,
HSP90↓,
annexin II↓, annexin II proteins directly bind to WA
m-FAM72A↓,
BCR-ABL↓,
Mortalin↓,
NRF2↓,
cMYB↓,
ROS↑, WA inhibits proliferation through ROS-mediated intrinsic apoptosis
ChemoSen↑, WA and cisplatin, WA produced ROS, while cisplatin caused DNA damage, suggesting that lower doses of cisplatin combined with suboptimal doses of WA could achieve the same effect
eff↑, sulforaphane and WA showed synergistic effects on epigenetic modifiers and cell proliferation in breast cancer cells
ChemoSen↑, WA and sorafenib caused G2/M arrest in anaplastic and papillary thyroid cancer cells
ChemoSen↑, combination of WA and 5-FU executed PERK axis-mediated endoplasmic reticulum (ER) stress-induced autophagy and apoptosis
eff↑, WA and carnosol also exhibit a synergistic effect on pancreatic cancer
*BioAv↓, Saurabh by Saurabh et al and Tianming et al reported oral bioavailability values 1.8% and 32.4 ± 4.8%, respectively, in male rats.
ROCK1↓, In another study, WA reduces macrophage infiltration and inhibits the expression of protein tyrosine kinase-2 (Pyk2), rho-associated kinase 1 (ROCK1), and VEGF in a hepatocellular carcinoma xenograft model, thereby suppressing tumor invasion and angi
TumCI↓,
Sp1/3/4↓, Furthermore, WA exerts potent anti-angiogenic activity in vivo.174 In the Ehrlich ascites tumor model, WA exerts its anti-angiogenic activity by reducing the binding of the transcription factor specificity protein 1 (Sp1) to VEGF
VEGF↓, n another study, WA reduces macrophage infiltration and inhibits the expression of protein tyrosine kinase-2 (Pyk2), rho-associated kinase 1 (ROCK1), and VEGF in a hepatocellular carcinoma xenograft model, thereby suppressing tumor invasion and angio
Hif1a↓, Furthermore, WA suppresses the AK4-HIF-1α signaling axis and acts as a potent antimetastatic agent in lung cancer.Citation79
EGFR↓, WA synergistically inhibited wild-type epidermal growth factor receptor (EGFR) lung cancer cell viability

1181- Ash,    Withaferin A inhibits Epithelial to Mesenchymal Transition in Non-Small Cell Lung Cancer Cells
- in-vitro, Lung, A549 - in-vitro, Lung, H1299
TumCMig↓,
TumCI↓,
EMT↓,
p‑SMAD2↓,
p‑SMAD3↓,
p‑NF-kB↓,

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.

5172- Ash,    Withaferin-A suppress AKT induced tumor growth in colorectal cancer cells
Akt↓, WA, a natural compound, resulted in significant inhibition of AKT activity and led to the inhibition of cell proliferation, migration and invasion
TumCP↓,
TumCMig↓,
TumCI↓,
EMT↓, by downregulating the epithelial to mesenchymal transition (EMT) markers in CRC cells overexpressing AKT
Snail↓, Further, significant inhibition of some important EMT markers, i.e., Snail, Slug, β-catenin and vimentin, was observed in WA-treated human CRC cells overexpressing AKT
Slug↓,
β-catenin/ZEB1↓,
Vim↓,
angioG↓, Significant inhibition of micro-vessel formation and the length of vessels were evident in WA-treated tumors, which correlated with a low expression of the angiogenic marker RETIC

5384- AsP,  MEL,    Synergistic Anticancer Effect of Melatonin and Ascorbyl Palmitate Nanoformulation: A Promising Combination for Cancer Therapy
- in-vivo, Var, NA
AntiCan↑, assess the anticancer effect of melatonin (MEL) and ascorbyl palmitate-loaded pluronic nanoparticles (APnp) combination on Ehrlich ascites carcinoma (EAC)-bearing mice.
TumCG↓, MEL alone showed a decrease in tumor growth by 48%, while in the case of using MEL combined with APnp, it displayed inhibition of tumor growth by 62%
Apoptosis↑, It also induced apoptosis and DNA damage.
DNAdam↑,
TumCCA↑, Besides, mediated cell cycle arrest.
IL6↓, IL-6/STAT3 pathway was inactivated to a greater extent after our combination treatment.
STAT3↓,
TumCP↓, antiproliferative effect of MEL and APnp via decreased expression of Ki-67
Ki-67↓,
TumCI↓, Our combination of MEL and APnp was able to inhibit cancer cell invasion and metastasis by decreasing the protein expression of MMP-9.
TumMeta↓,
MMP9↓,
eff↑, The synergy score was 21.06 ( > 10 indicates synergistic effect)
*Catalase↑, Administration of MEL alone or MEL+ APnp treated mice showed a significant and highly significant increase, respectively (P<0.05, P<0.01) in the antioxidant enzyme activities of CAT and SOD, and GSH.
*SOD↑,
*GSH↑,
*MDA↓, Figure 2 demonstrated a highly significant and extremely significant reduction, respectively (P<0.01, P<0.001) in the MDA and NO levels compared to the EAC control group.
*NO↓,
*antiOx↑, Figure 2 demonstrated a highly significant and extremely significant reduction, respectively (P<0.01, P<0.001) in the MDA and NO levels compared to the EAC control group.
*hepatoP↑, combined MEL and APnp- treated animals displayed a noteworthy amelioration for all examined organs when compared to the control EAC inoculated group, Figure 3.
*RenoP↑,

4820- ASTX,    Astaxanthin suppresses the malignant behaviors of nasopharyngeal carcinoma cells by blocking PI3K/AKT and NF-κB pathways via miR-29a-3p
- in-vitro, NPC, NA
TumCP↓, C666-1 cell proliferation, invasion, and migration were significantly suppressed by astaxanthin while cell apoptosis and cell cycle arrest at G1 phase were effectively enhanced in the context of 10 mg/mL astaxanthin.
TumCI↓,
Apoptosis↑,
TumCCA↑,
cycD1/CCND1↓, inhibitory effect of astaxanthin on Cyclin D1 and Bcl-2 protein levels as well as the promoting impact of astaxanthin on p21 and Bax were also amplified in combination with LY294002 or PTL treatment.
Bcl-2↓,
P21↑,
BAX↑,
PI3K↓, Astaxanthin significantly suppresses NPC cell proliferation, cell cycle arrest, migration, invasion while promoting cell apoptosis by inactivating PI3K/AKT and NF-κB pathways.
Akt↓,
NF-kB↓,
miR-29b↑, Astaxanthin upregulates miR-29a-3p expression to inactivate the PI3K/AKT and NF-κB pathways

4808- ASTX,    Anti-Tumor Effects of Astaxanthin by Inhibition of the Expression of STAT3 in Prostate Cancer
- in-vitro, Pca, DU145 - in-vivo, NA, NA
TumCP↓, Astaxanthin resulted in suppression of the proliferation of DU145 cells and the level of STAT3.
STAT3↓, Thus, astaxanthin inhibits the proliferation of DU145 cells by reducing the expression of STAT3.
Apoptosis↑, treatment of DU145 cells with astaxanthin decreased the cloning ability, increased the apoptosis percentage and weakened the abilities of migration and invasion of the cells.
TumCMig↓,
TumCI↓,

5362- AV,    Anti-cancer effects of aloe-emodin: a systematic review
- Review, Var, NA
AntiCan↑, Aloe-emodin possesses multiple anti-proliferative and anti-carcinogenic properties in a host of human cancer cell lines, with often multiple vital pathways affected by the same molecule.
eff↝, The effects of aloe-emodin are not ubiquitous across all cell lines but depend on cell type.
TumCP↓, most notable effects include inhibition of cell proliferation, migration, and invasion; cycle arrest; induction of cell death;
TumCMig↓,
TumCI↓,
TumCCA↑,
TumCD↑,
MMP↓, mitochondrial membrane and redox perturbations; and modulation of immune signaling.
ROS↑, which coincide with deleterious effects on mitochondrial membrane permea-bility and/or oxidative stress via exacerbated ROS production.
Apoptosis↑, In bladder cancer cells (T24), aloe-emodin induced time-and dose-dependent apoptosis [7]
CDK1↓, reduced levels of cyclin-dependent kinase (CDK) 1, cyclin B1, and BCL-2 after treatment with aloe-emodin.
CycB/CCNB1↓,
Bcl-2↓,
PCNA↓, Increases in cyclin B1, CDK1, and alkaline phosphatase (ALP) activity were observed along with inhibition of proliferating cell nuclear antigen (PCNA), showing decreased proliferation.
ATP↓, human lung non-small cell car¬cinoma (H460). They found a time- de¬pendent reduction in ATP, lower ATP synthase expression
ER Stress↑, hypothesized to cause apoptosis by augmenting endoplasmic reticulum stress [16].
cl‑Casp3↑, (HepG2) cells underwent apoptosis through a cas-pase-dependent pathway with cleavage and activation of caspases-3/9 and cleavage of PARP [24]
cl‑Casp9↑,
cl‑PARP↑,
MMP2↓, Matrix metalloproteinase-2 was significantly decreased, with an increase in ROS and cytosolic calcium.
Ca+2↑,
DNAdam↑, U87 malignant glioma cells through disruption of mitochondrial membrane potential, cell cycle arrest in the S phase, and DNA fragmentation in a time-dependent manner with minimal necrosis
Akt↓, Prostate cancer. Following treatment with aloe-emodin, mTORC2's down¬stream enzymes, AKT and PKCa, were inhibited
PKCδ↓,
mTORC2↓, Proliferation of PC3 cells was inhibited as a result of aloe-emodin binding to mTORC2, with inhibition of mTORC2 kinase activity.
GSH↓, Skin cancer. Intracellular ROS increased, while intra-cellular-reduced glutathione (GSH) was depleted and BCL-2 (anti-apoptotic protein) was down-regulated.
ChemoSen↑, Aloe-emodin also sensitizes skin cancer cells to chemo-therapy. aloe-emodin and emodin potentiated the therapeutic effects of cisplatin, doxo-rubicin, 5-fluorouracil

5250- Ba,    Exploring baicalein: A natural flavonoid for enhancing cancer prevention and treatment
- Review, Var, NA
Apoptosis↑, Baicalein is thought to prevent cancer progression by inducing apoptosis, autophagy, and genome instability, and its ability to promote chemo-potentiation, anti-metastatic effects, and regulate specific signalling molecules and transcription factors.
TumAuto↑,
DNAdam↑,
*antiOx↑, Baicalein has already been proven to be a radical scavenger that acts as an antioxidant [14,15
Inflam↓, it can also reduce inflammation [16] and act as an E2 prostaglandin inhibitor [17].
PGE2↓,
TumCCA↑, Baicalein properties prevent cell proliferation, induce apoptosis, autophagy, cell cycle arrest, cancer cell migration and invasion, and decrease angiogenesis [18,19].
TumCMig↓,
TumCI↓,
angioG↓,
selectivity↑, Furthermore, some studies have suggested that baicalein has a lower toxicity on normal cells than cancer cells, indicating some selectivity for cancer cells.
ChemoSen↑, the current review emphasises baicaleins' synergistic potential with other chemotherapeutic agents
HIF-1↓, baicalein against ovarian cancer by demonstrating that it can limit tumour cell viability by downregulating the expression of cancer-promoting genes such as HIF-1, cMyc, NFkB, and VEGF
cMyc↓,
NF-kB↓,
VEGF↓,
P53↑, Baicalein has been shown to activate p53, a tumour suppressor protein that regulates cell growth and division [26].
MMP2↓, anticancer properties of baicalein are mediated through various molecular mechanisms, including inhibition of MMP-2;
CSCs↓, inhibition of cancer stem cells
Bcl-xL↓, after bladder cancer cells were treated with baicalein, the expression of antiapoptotic genes (Bcl2, Bcl-xL, XIAP, and survivin) was reduced, and cell viability was decreased [38].
XIAP↓,
survivin↓,
tumCV↓,
Casp3↑, upregulating the expression of caspase-3 and caspase-8 and decreased the BCL-2/BAX ratio [16]
Casp8↑,
Bax:Bcl2↑,
Akt↓, in lung cancer cells, apoptosis was induced through the downregulation of the Akt/mTOR signalling pathway [25].
mTOR↓,
PCNA↓, baicalein treatment promoted apoptosis in mice with U87 gliomas by downregulating PCNA expression, enhancing the expression of caspase-3 and caspase-9 and improving the Bax/Bcl-2 ratio
MMP↓, baicalein treatment of lung cancer cells caused a collapse of the mitochondrial membrane potential (MMP), an increase in ROS generation, and enhanced PARP, caspase 3, and caspase 9 cleavage,
ROS↑,
PARP↑,
Casp9↑,
BioAv↑, Baicalein has been found to enhance the cytotoxicity and bioavailability of certain cancer therapy drugs when combined [85]
eff↑, combination of baicalein with silymarin differentially decreased the viability of HepG2 cells, enhanced the proportion of cells in the G0/G1 phase, upregulated tumour suppressors such as Rb and p53 and CDK inhibitors, and downregulated cyclin D1, cyc
P-gp↓, By inhibiting P-glycoprotein (P-gp), baicalein can increase the accumulation of chemotherapeutic drugs within cancer cells [21]
BioAv↑, selenium–baicalein nanoparticles as a targeted therapeutic strategy for NSCLC. This strategy significantly improves the bioavailability of baicalein through several mechanisms.
selectivity↑, ome studies have suggested that baicalein has a lower toxicity on normal cells than cancer cells, indicating some selectivity for cancer cells

5251- Ba,    The Fascinating Effects of Baicalein on Cancer: A Review
- Review, Var, NA
AntiTum↑, The anti-tumor functions of baicalein are mainly due to its capacities to inhibit complexes of cyclins to regulate the cell cycle, to scavenge oxidative radicals, to attenuate mitogen activated protein kinase (MAPK), protein kinase B (Akt) or mammali
TumCCA↓,
ROS↓,
MAPK↓,
Akt↓,
mTOR↓,
Casp3↑, , to induce apoptosis by activating caspase-9/-3 and to inhibit tumorinvasion and metastasis by reducing the expression of matrix metalloproteinase-2/-9 (MMP-2/-9).
Casp9↑,
TumCI↓,
TumMeta↓,
MMP2↓,
MMP9↓,
Securin↓, Baicalein also induced cell death by reducing the expression of securin, while also inhibiting cancer cell death by affecting the expression of p-AKT and γ-H2AX [26].
γH2AX↝,
N-cadherin↓, Baicalein also decreased the expression of metastasis-associated molecules, including N-cadherin, vimentin, ZEB1, and ZEB2.
Vim↓,
Zeb1↓,
ZEB2↓,
TumCMig↓, researchers demonstrated that baiclalein inhibited cellular adhesion, migration, invasion, and growth of HCC cells both in vitro and in vivo.
TumCG↑,
12LOX↓, Baicalein is an inhibitor of 12-LOX and induced apoptosis, morphological changes, and carbonic anhydrase expression in PaCa cells.
DR5↑, Baicalein lessened this resistance to TRAIL by upregulating DR5 expression and promoting the expression of ROS, thus causing TRAIL sensitization in PC3 cells [85]
ROS↑,
RadioS↑, baicalein increased the sensitivity of prostate cancer cells to radiation without affecting this sensitivity in normal cells
ChemoSen↑, Combination therapy of baicalein with paclitaxel, which were assembled by nanoparticles, was demonstrated to have synergistic anticancer effects in A549 lung cancer cells and in mice bearing A549/PTX drug-resistant lung cancer xenografts [97].
BioAv↓, It is worth noting that the bioavailability of baicalein in vivo remains low.

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

2296- Ba,    The most recent progress of baicalein in its anti-neoplastic effects and mechanisms
- Review, Var, NA
CDK1↓, graphical abstract
Cyc↓,
p27↑,
P21↑,
P53↑,
TumCCA↑, Cell cycle arrest
TumCI↓, Inhibit invastion
MMP2↓,
MMP9↓,
E-cadherin↑,
N-cadherin↓,
Vim↓,
LC3A↑,
p62↓,
p‑mTOR↓,
PD-L1↓,
CAFs/TAFs↓,
VEGF↓,
ROCK1↓,
Bcl-2↓,
Bcl-xL↓,
BAX↑,
ROS↑,
cl‑PARP↑,
Casp3↑,
Casp9↑,
PTEN↑, A549, H460
MMP↓, ↓mitochondrial transmembrane potential, redistribution of cytochrome c,
Cyt‑c↑,
Ca+2↑, ↑Ca2+
PERK↑, ↑PERK, ↑IRE1α, ↑CHOP,
IRE1↑,
CHOP↑,
Copper↑, ↑Cu+2
Snail↓, ↓Snail, ↓vimentin, ↓Twist1,
Vim↓,
Twist↓,
GSH↓, ↑ROS, ↓GSH, ↑MDA, ↓MMP, ↓NRF2, ↓HO-1, ↓GPX4, ↓FTH1, ↑TFR1, ↓p-JAK2, ↓p-STAT3
NRF2↓,
HO-1↓,
GPx4↓,
XIAP↓, ↓Bcl-2, ↓Bcl-xL, ↓XIAP, ↓surviving
survivin↓,
DR5↑, ↑ROS, ↑DR5

5536- BBM,    Regulation of Cell-Signaling Pathways by Berbamine in Different Cancers
- Review, Var, NA
JAK↝, In this review, we comprehensively analyze how berbamine modulates deregulated pathways (JAK/STAT, CAMKII/c-Myc) in various cancers.
STAT3↓, Berbamine physically interacted with STAT3 and inhibited its activation [8].
p‑CaMKII ↓, An orally administered, bioactive small molecule analog of berbamine, tosyl chloride-berbamine (TCB), considerably reduced phosphorylated levels of CaMKIIγ
TGF-β↑, berbamine induces activation of the TGF/SMAD pathway for the effective inhibition of cancer progression.
Smad1↑,
ChemoSen↑, Berbamine enhanced the chemosensitivity of gefitinib against PANC-1 and MIA PaCa-2 cancer cells [8].
RadioS↑, Moreover, berbamine and radiation effectively induced a regression of the tumors in mice subcutaneously injected with FaDu cells [10].
TumCI↓, berbamine-GMO-TPGS nanoparticles showed superior cellular toxicity, as well as an inhibition of migration and invasion in metastatic breast cancer MDA-MB-231,
TumCMig↓,
ROS↑, Berbamine increased the intracellular ROS levels via the downregulation of antioxidative genes such as NRF2, SOD2, GPX-1 and HO-1.
NRF2↓,
SOD2↓,
GPx1↓,
HO-1↓,

5540- BBM,    Berbamine Inhibits Cell Proliferation and Migration and Induces Cell Death of Lung Cancer Cells via Regulating c-Maf, PI3K/Akt, and MDM2-P53 Pathways
- vitro+vivo, NSCLC, NA
TumCMig↓, BBM (10 μM) also significantly inhibited the migration and invasion ability of cancer cells in wound scratch and Transwell assays.
TumCI↓,
PI3K↓, BBM inhibited the PI3K/Akt and MDM2-p53 signaling pathways, and BBM downregulated the expression of c-Maf.
Akt↓,
MDM2↓,
TumCP↓, Our results show that BBM inhibits proliferation and metastasis and induces cell death of lung cancer cells in vitro and in vivo.
TumMeta↓,

5555- BBM,    Berbamine inhibits cell proliferation and invasion by increasing FTO expression in renal cell carcinoma cells
- vitro+vivo, RCC, NA
TumCP↓, BBM effectively inhibited the proliferation, migration and invasion of RCC cells in a dose-dependent manner
TumCMig↓,
TumCI↓,
TumCG↓, and BBM also significantly inhibited the growth of tumor in vivo,
toxicity↓, which has fewer toxic effects on the other organs.
FTO↑, mechanistic studies showed that BBM significantly promoted the expression of FTO mRNA and protein in RCC cells,

2700- BBR,    Cell-specific pattern of berberine pleiotropic effects on different human cell lines
- in-vitro, GBM, U343 - in-vitro, GBM, MIA PaCa-2 - in-vitro, Nor, HDFa
selectivity↑, berberine differentially affects cell viability, displaying a higher cytotoxicity on the two cancer cell lines than on HDF
TumCCA↑, Berberine also affects cell cycle progression, senescence, caspase-3 activity, autophagy and migration in a cell-specific manner.
Casp3↑, it increases caspase-3 activity and impairs migration/invasion.
TumCI↓,
TumCMig↓,
N-cadherin?,
DNMT1↑, DNMT1 was also upregulated in U343 cells (4-fold) after 50 μM berberine for 48 hours and in MIA PaCa-2 cells after treatment with both 10 μM and 50 μM berberine for 48 hours (5-fold and 15-fold, respectively).

2694- BBR,    Berberine down-regulates IL-8 expression through inhibition of the EGFR/MEK/ERK pathway in triple-negative breast cancer cells
- in-vitro, BC, NA
IL8↓, BBR dramatically suppresses IL-8 expression.
TumCI↓, BBR also inhibited cell invasiveness
EGFR↓, BBR down-regulates EGFR protein expression and dose-dependently inhibits MEK and ERK phosphorylation.
MEK↓,
ERK↓,
TGF-β1↓, BBR inhibits the tumorigenic and angiogenic properties of TNBC cells by inhibiting TGF-β1 expression and VEGF secretion (
VEGF↓,


Showing Research Papers: 1 to 50 of 320
Page 1 of 7 Next

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 320

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Copper↑, 1,   Ferroptosis↑, 3,   GPx1↓, 1,   GPx4↓, 2,   GSH↓, 4,   H2O2↑, 1,   HO-1↓, 2,   Keap1↑, 1,   lipid-P↑, 1,   MDA↑, 2,   NADH↓, 1,   NRF2↓, 5,   ROS↓, 1,   ROS↑, 17,   SOD2↓, 1,   xCT↓, 1,  

Metal & Cofactor Biology ⓘ

Ferritin↓, 1,   Tf↑, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 2,   BCR-ABL↓, 1,   MEK↓, 1,   p‑MEK↓, 1,   MMP↓, 6,   MMP↑, 1,   Mortalin↓, 1,   XIAP↓, 2,  

Core Metabolism/Glycolysis ⓘ

12LOX↓, 2,   AMPK↑, 6,   cMyc↓, 3,   FASN↓, 2,   FDG↓, 1,   GAPDH↓, 1,   GlucoseCon↓, 1,   PDH↑, 1,   PIK3CA↓, 1,   PKM2↓, 1,   p‑S6↓, 1,   SIRT1↓, 1,   SIRT1↑, 1,   SREBP1↓, 1,  

Cell Death ⓘ

Akt↓, 13,   p‑Akt↓, 3,   APAF1↑, 1,   Apoptosis↑, 17,   Bak↑, 1,   BAX↑, 6,   Bax:Bcl2↑, 3,   Bcl-2↓, 8,   Bcl-xL↓, 5,   Casp↑, 3,   Casp2↑, 1,   Casp3↑, 9,   cl‑Casp3↑, 2,   cl‑Casp7↑, 1,   Casp8↑, 2,   cl‑Casp8↑, 1,   Casp9↑, 7,   cl‑Casp9↑, 2,   CK2↓, 2,   Cyt‑c↑, 5,   DR5↑, 2,   Fas↑, 2,   Ferroptosis↑, 3,   cl‑IAP2↑, 1,   JNK↓, 1,   JNK↑, 2,   p‑JNK↓, 1,   MAPK↓, 2,   MDM2↓, 1,   p27↑, 1,   survivin↓, 3,   Telomerase↓, 1,   TumCD↑, 1,  

Kinase & Signal Transduction ⓘ

p‑CaMKII ↓, 1,   HER2/EBBR2↓, 1,   Sp1/3/4↓, 2,  

Transcription & Epigenetics ⓘ

other↓, 1,   other↑, 2,   other↝, 1,   p‑pRB↓, 1,   tumCV↓, 2,  

Protein Folding & ER Stress ⓘ

CHOP↑, 2,   ER Stress↑, 3,   HSP90↓, 3,   HSPs↓, 1,   IRE1↑, 1,   PERK↑, 1,  

Autophagy & Lysosomes ⓘ

Beclin-1↑, 1,   LC3A↑, 1,   p62↓, 1,   TumAuto↑, 4,  

DNA Damage & Repair ⓘ

DNAdam↑, 5,   DNMT1↑, 1,   m-FAM72A↓, 1,   P53↓, 1,   P53↑, 8,   PARP↑, 1,   cl‑PARP↑, 4,   PCNA↓, 2,   γH2AX↝, 1,  

Cell Cycle & Senescence ⓘ

CDK1↓, 4,   CDK1↑, 1,   CDK2↑, 1,   CDK4↓, 1,   CDK4↑, 1,   Cyc↓, 1,   cycA1/CCNA1↓, 1,   CycB/CCNB1↓, 2,   cycD1/CCND1↓, 1,   P21↑, 6,   Securin↓, 1,   TumCCA↓, 1,   TumCCA↑, 19,  

Proliferation, Differentiation & Cell State ⓘ

CD133↓, 1,   CD24↓, 1,   CD44↓, 1,   cMYB↓, 1,   CSCs↓, 4,   Diff↑, 1,   EMT↓, 13,   ERK↓, 4,   ERK↝, 1,   p‑ERK↓, 1,   p‑GSK‐3β↓, 1,   IGF-1↓, 1,   IGFBP3↑, 1,   mTOR↓, 8,   mTOR↑, 1,   p‑mTOR↓, 1,   mTORC2↓, 1,   Nanog↓, 1,   NOTCH1↓, 1,   NOTCH3↓, 1,   OCT4↓, 1,   p‑P70S6K↓, 1,   p‑P90RSK↑, 1,   PI3K↓, 8,   p‑PI3K↓, 1,   PTEN↑, 1,   SOX2↓, 1,   STAT3↓, 6,   TCF↓, 1,   TumCG↓, 11,   TumCG↑, 1,   Wnt↓, 2,   Wnt/(β-catenin)↓, 4,   ZFX↓, 1,  

Migration ⓘ

annexin II↓, 1,   AntiAg↑, 2,   Ca+2↑, 5,   CAFs/TAFs↓, 1,   cal2↑, 1,   E-cadherin↑, 8,   FAK↓, 1,   FTO↑, 1,   ITGB4↓, 2,   Ki-67↓, 2,   LEF1↓, 1,   miR-133a-3p↑, 1,   miR-29b↑, 1,   MMP17↓, 1,   MMP2↓, 9,   MMP9↓, 9,   MMPs↓, 2,   N-cadherin?, 1,   N-cadherin↓, 5,   NEDD9↓, 1,   PDGF↓, 1,   PKCδ↓, 1,   ROCK1↓, 2,   Slug↓, 2,   Smad1↑, 1,   p‑SMAD2↓, 3,   p‑SMAD3↓, 1,   Snail↓, 4,   talin?, 1,   TGF-β↓, 3,   TGF-β↑, 1,   TGF-β1↓, 1,   TIMP1↓, 1,   TIMP2↓, 1,   TumCI↓, 50,   TumCMig↓, 36,   TumCP↓, 26,   TumMeta↓, 10,   Twist↓, 3,   uPA↓, 2,   Vim↓, 11,   Vim↑, 1,   Zeb1↓, 1,   ZEB2↓, 1,   β-catenin/ZEB1↓, 6,  

Angiogenesis & Vasculature ⓘ

angioG↓, 6,   angioG↑, 1,   ATF4↑, 1,   EGFR↓, 5,   p‑EGFR↓, 1,   EGR4↓, 1,   HIF-1↓, 1,   Hif1a↓, 5,   Hif1a↑, 1,   TXA2↓, 1,   VEGF↓, 10,  

Barriers & Transport ⓘ

GLUT1↓, 1,   P-gp↓, 2,  

Immune & Inflammatory Signaling ⓘ

COX1↓, 1,   COX2↓, 1,   ICAM-1↓, 1,   IKKα↓, 1,   p‑IKKα↓, 1,   IL1α↓, 1,   IL1β↓, 1,   IL6↓, 2,   IL8↓, 1,   Imm↑, 1,   Inflam↓, 2,   JAK↝, 1,   MCP1↓, 1,   NF-kB↓, 5,   p‑NF-kB↓, 1,   p‑NF-kB↑, 1,   p65↓, 1,   PD-L1↓, 2,   PGE2↓, 2,   PSA↓, 1,   TNF-α↓, 1,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,   CDK6↑, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   BioAv↑, 2,   BioAv↝, 2,   ChemoSen↑, 11,   Dose↑, 1,   Dose↝, 1,   Dose∅, 1,   eff↑, 10,   eff↝, 2,   Half-Life↓, 1,   RadioS↑, 4,   selectivity↑, 7,  

Clinical Biomarkers ⓘ

AR↓, 1,   EGFR↓, 5,   p‑EGFR↓, 1,   Ferritin↓, 1,   HER2/EBBR2↓, 1,   IL6↓, 2,   Ki-67↓, 2,   PD-L1↓, 2,   PSA↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 2,   AntiTum↑, 3,   chemoPv↑, 1,   OS↑, 1,   QoL↑, 1,   Symptoms↓, 1,   toxicity↓, 3,   toxicity↑, 1,  
Total Targets: 257

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 3,   Catalase↑, 1,   GSH↑, 2,   lipid-P↓, 1,   MDA↓, 1,   NRF2↑, 1,   ROS↓, 1,   SOD↑, 1,  

Metal & Cofactor Biology ⓘ

IronCh↑, 1,  

Core Metabolism/Glycolysis ⓘ

GlucoseCon↑, 1,  

Cell Death ⓘ

MAPK↓, 1,  

Transcription & Epigenetics ⓘ

Ach↑, 1,   other↓, 1,   other↝, 1,  

Migration ⓘ

PKCδ↓, 1,  

Angiogenesis & Vasculature ⓘ

NO↓, 1,  

Immune & Inflammatory Signaling ⓘ

IL1β↓, 1,   IL6↓, 1,   Inflam↓, 1,  

Synaptic & Neurotransmission ⓘ

ChAT↑, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 2,   BioAv↑, 2,   BioAv↝, 1,   Half-Life↓, 1,   Half-Life∅, 1,  

Clinical Biomarkers ⓘ

IL6↓, 1,  

Functional Outcomes ⓘ

hepatoP↑, 2,   memory↑, 1,   neuroP↑, 1,   RenoP↑, 1,   toxicity↓, 5,  
Total Targets: 31

Scientific Paper Hit Count for: TumCI, Tumor Cell invasion
14 Curcumin
13 Resveratrol
13 Quercetin
12 Shikonin
11 Berberine
10 Apigenin (mainly Parsley)
10 Honokiol
10 Sulforaphane (mainly Broccoli)
9 EGCG (Epigallocatechin Gallate)
8 Thymoquinone
7 Ashwagandha(Withaferin A)
7 Betulinic acid
7 Chlorogenic acid
7 Magnetic Fields
6 Fisetin
6 Garcinol
6 Magnolol
6 Piperlongumine
5 Astragalus
5 Lycopene
5 Metformin
5 Pterostilbene
4 Artemisinin
4 Baicalein
4 Carvacrol
4 Celastrol
4 Gemcitabine (Gemzar)
4 Chrysin
4 Phenethyl isothiocyanate
4 Rosmarinic acid
4 Silymarin (Milk Thistle) silibinin
4 Urolithin
3 Silver-NanoParticles
3 Alpha-Lipoic-Acid
3 Berbamine
3 Brucea javanica
3 brusatol
3 Propolis -bee glue
3 Gambogic Acid
3 Juglone
3 Magnetic Field Rotating
3 Bicarbonate(Sodium)
3 Piperine
3 Whole Body Vibration
2 Astaxanthin
2 Boswellia (frankincense)
2 Capsaicin
2 Caffeic Acid Phenethyl Ester (CAPE)
2 Celecoxib
2 Disulfiram
2 Copper and Cu NanoParticles
2 Ellagic acid
2 Emodin
2 Ginkgo biloba
2 Genistein (soy isoflavone)
2 Graviola
2 Grapeseed extract
2 HydroxyTyrosol
2 Nimbolide
2 Cisplatin
2 salinomycin
2 Sulfasalazine
2 Selenite (Sodium)
2 Aflavin-3,3′-digallate
2 Vitamin C (Ascorbic Acid)
1 3-bromopyruvate
1 Ajoene (compound of Garlic)
1 alpha Linolenic acid
1 Andrographis
1 Aspirin -acetylsalicylic acid
1 Ascorbyl Palmitate
1 Melatonin
1 Aloe anthraquinones
1 Biochanin A
1 Atorvastatin
1 bempedoic acid
1 Bufalin/Huachansu
1 Bacopa monnieri
1 Boron
1 Carnosic acid
1 chitosan
1 Selenium NanoParticles
1 Chlorophyllin
1 Cinnamon
1 Cyclopamine
1 Deguelin
1 Evodiamine
1 Ferulic acid
1 Paclitaxel
1 γ-linolenic acid (Borage Oil)
1 Proanthocyanidins
1 Hydrogen Gas
1 Hydroxycinnamic-acid
1 Luteolin
1 5-fluorouracil
1 doxorubicin
1 immunotherapy
1 Noscapine
1 Oroxylin A
1 Oleuropein
1 Orlistat
1 Psoralidin
1 isoflavones
1 Docetaxel
1 Hyperoside
1 Germacranolide
1 Radiotherapy/Radiation
1 Salvia miltiorrhiza
1 Thymol-Thymus vulgaris
1 Ursolic acid
1 Arsenic trioxide
1 Vitamin K2
1 VitK3,menadione
1 Zinc
1 β‐Elemene
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#:324  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

 

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