TumCP Cancer Research Results
TumCP, Tumor Cell proliferation: Click to Expand ⟱
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Tumor cell proliferation is a key characteristic of cancer. It refers to the rapid and uncontrolled growth of cells that can lead to the formation of tumors.
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Scientific Papers found: Click to Expand⟱
TumCP↓, We report here the anti-proliferative activity against human leukaemia cells K562, THP-1, CCRF-CEM and CCRF-CEM/C1 and the inhibitory mechanism on human topoisomerases I and II
TOP1↓,
TOP2↓,
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in-vitro, |
Melanoma, |
A431 |
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in-vitro, |
OS, |
MG63 |
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in-vitro, |
Nor, |
HaCaT |
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TumCP↓, HE has showed increased anti-proliferative effect against the cancer cells but was resisted by non-malignant cells.
selectivity↑,
AntiCan↑, 1,8-Cineole has shown potential anti-cancer activity in a dose-dependent manner, and cell death was induced through ROS-mediated apoptosis.
TumCD↑,
Apoptosis↑,
Dose↝, 10 mg mL-1 concentration was able to cause >45% cell death in A431 and >20% in MG-63, as against only about 6% in HaCaT cells.
ROS↑, HE-C increased ROS production in cancer cells
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vitro+vivo, |
Colon, |
HCT116 |
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TumCP↓, anti-proliferative effect of 1, 8-cineole on human colon cancer cell lines HCT116 and RKO by WST-8 and BrdU assays.
Apoptosis↑, Specific induction of apoptosis, not necrosis, was observed in human colon cancer cell lines HCT116 and RKO by 1, 8-cineole.
survivin↓, 1, 8-cineole was associated with inactivation of survivin and Akt and activation of p38.
Akt↓,
p38↑,
cl‑PARP↑, induced cleaved PARP and caspase-3, finally causing apoptosis.
cl‑Casp3↑,
TumVol↓, 1, 8-cineole inhibits tumor growth of RKO xenografts.
ChemoSen↑, 2DG and sorafenib in combination suppressed the proliferation and motility of HCC cells more effectively than 2DG or sorafenib alone,
TumCP↓, In the present study, 3 µM 2DG and 30 µM sorafenib significantly suppressed the proliferation of HLF and HCC PLC/PRF/5 cells.
cycD1/CCND1↓, Sorafenib and 2DG independently decrease cyclin D1 expression
MMP9↓, expression of MMP9 significantly decreased when cells were treated with a combination of 2DG and sorafenib compared with 2DG or sorafenib alone
eff↑, Upon oral administration of 3-BP-based agent KAT-101, the 3-BP derivative, being structurally similar to lactic acid, specifically binds to and enters cancer cells through monocarboxylic acid transporters (MCTs)
Glycolysis↓, KAT-101 interferes with both glycolysis and mitochondrial oxidative phosphorylation (OxPhos), thereby depleting adenosine triphosphate (ATP) levels and thus limits energy supply needed by cancer cells to proliferate.
OXPHOS↓,
ATP↓,
TumCP↓,
Apoptosis↑, This induces cancer cell apoptosis and prevents cancer cell proliferation.
HK2↓, In addition, KAT-101 is able to release mitochondrial-bound hexokinase (HK) II (HK2)
MPT↑, increases the formation of mitochondrial permeability transition pores (MPTPs), which induces apoptosis.
LDH↓, KAT-101 also inhibits a variety of enzymes, including lactate dehydrogenase (LDH), pyruvate dehydrogenase (PDH) and pyruvate dehydrogenase kinase (PDHK).
PDH↓,
TrxR↓, Auranofin mainly targets the anti-oxidative system catalyzed by thioredoxin reductase (TrxR), which protects the cell from oxidative stress and death in the cytoplasm and the mitochondria.
ROS↑, Inhibiting TrxR dysregulates the intracellular redox state causing increased intracellular reactive oxygen species levels, and stimulates cellular demise
eff↑, TrxR is over-expressed in many cancers as an adaptive mechanism for cancer cell proliferation, rendering it an attractive target for cancer therapy, and auranofin as a potential therapeutic agent for cancer.
Apoptosis↑, promotion of ASK-induced apoptosis, and blockage of cell growth, proliferation, and survival due to reduced AKT activity and NF-kB- and p53-mediated transcription.
TumCG↓,
TumCP↓,
Akt↓,
NF-kB↓,
DNAdam↑, DNA damage
eff↝, auranofin inhibits TrxR1 in a p53-independent manner
eff↓, Pre-treatment with NAC counteracted the cancer cell killing effects of auranofin,
PI3K↓, auranofin induces cytotoxicity in human pancreatic adenocarcinoma and non-small cell lung cancer via the inhibition of the PI3K/AKT/mTOR pathway
Akt↓,
mTOR↓,
Hif1a↓, auranofin inhibits the cancer cell response to hypoxia, demonstrated by a decrease in HIF-1 𝛼 expression and VEGF secretion upon auranofin treatment under hypoxic conditions
VEGF↓,
Casp3↑, auranofin was shown to induce caspase-3-mediated apoptosis in human ovarian carcinoma SKOV-3 cells
CSCs↓,
ATP↓, it was found that auranofin inhibits ABCG2 function by depleting cellular ATP via inhibition of glycolysis [96]
Glycolysis↓,
eff↑, auranofin synergizes with another Trx1 inhibitor, piperlongumine, in killing gastric cancer cells in association with ROS-mediated ER stress response and mitochondrial dysfunction.
eff↑, when the gold complex is combined with either selenite or tellurite [104]
MMP↓, Increased ROS induced by AUR causes decreased membrane potential in the mitochondrial membrane, resulting in a decrease in anti-apoptotic proteins, caspase-dependent cell death, and translocation of apoptosis-inducing factor (AIF)
AIF↑,
toxicity↓, Auranofin is considered safe for human use in treating rheumatoid arthritis; thus, this gold derivative can reach the clinic for other diseases relatively quickly and at a low cost
TrxR↓, Auranofin inhibits the activity of thioredoxin reductase (TrxR
ROS↑, TrxR inhibition leads to an increase in cellular oxidative stress and induces apoptosis
Apoptosis↓,
TumCP↓, TrxR1 knockdown also inhibits cancer cell proliferation and DNA replication
eff↑, cytotoxicity of cisplatin is increased in cells expressing high levels of TrxR1 compared with cells expressing low levels
TumCMig↓,
TumCI↓,
Ki-67↓,
TumCP↓,
Snail↓,
Vim↓,
E-cadherin↑,
Wnt↓,
β-catenin/ZEB1↓,
TumCP↓,
Apoptosis↑,
NF-kB↓,
p50↓,
cycD1/CCND1↓,
Bcl-xL↓,
ChemoSen↑, AS-IV can enhance paclitaxel-induced cell apoptosis and cell cycle arrest at G2/M phase
angioG↓,
ChemoSen↑, Enhances Sensitivity to Cisplatin
*Imm↑, AR possesses various biological functions, including potent immunomodulation, antioxidant, anti-inflammation and antitumor
activities.
*antiOx↑,
*Inflam↓,
AntiTum↑,
eff↑, characteristics of increasing curative effect and reducing the toxicity of chemotherapeutic drugs [11 , 118].
chemoP↑,
Dose↝, main bioactive compounds responsible for the anti-cancer effects of AR mainly include formononetin,
AS-IV and APS. S
TumCMig↓, AS-IV could inhibit the migration and proliferation of non-small cell lung cancer (NSCLC
TumCP↓,
Akt↓, h via inhibition of the Akt/GSK-3β/β-catenin
signaling axis.
GSK‐3β↓,
MMP2↓, downregulating the expression of matrix metalloproteases (MMP)-2 and -9
MMP9↓,
EMT↓, AS-IV could inhibit TGF-B1 induced EMT through inhibition of PI3K/AKT/NF-KB
PI3K↓,
Akt↓,
NF-kB↓,
Inflam↓,
TGF-β1↓,
TNF-α↓,
IL6↓,
Fas↓, reduced FAS/FasL
FasL↓,
NOTCH1↓, decressing notch1
JNK↓, inactivating JNK pathway [145]
TumCG↓, The results showed that the AR water extract could inhibit the growth of colorectal cancer in vivo without apparent toxicity and side effect, which suggests that AR is a potential therapeutic drug for colorectal cancer
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/SLC7A11↓,
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/ABCB1↓,
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/SREBF1↓,
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
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.
AntiCan↑, Preclinical studies indicate that APS exerts significant anti-liver cancer effects through multiple biological actions, including the promotion of apoptosis, inhibition of proliferation, suppression of epithelial–mesenchymal transition, regulation of
Apoptosis↑,
TumCP↓,
EMT↓,
Imm↑, improving host immune response
ChemoSen↑, APS exhibits synergistic effects when combined with conventional chemotherapeutics and interventional treatments such as transarterial chemoembolisation, improving efficacy and reducing toxicity.
BioAv↓, limitations such as low bioavailability and a lack of large-scale clinical trials remain challenges for clinical translation.
TumCG↓, APS significantly inhibited tumour growth in H22-bearing mice with a dose-dependent effect (100, 200, 400 mg/kg), with the 400 mg/kg group achieving a tumour inhibition rate of 59.01%
IL2↑, APS enhance the thymus and spleen indices and elevates the key cytokines, including IL-2, IL-12, and TNF-α.
IL12↑,
TNF-α↑,
P-gp/ABCB1↓, APS reversed chemoresistance by downregulating P-glycoprotein and MDR1 mRNA expression
MDR1↓,
QoL↑, These effects contributed to improved treatment tolerance and enhanced quality of life [39].
Casp↑, APS can activate both the intrinsic and extrinsic apoptotic pathways, leading to caspase activation and DNA fragmentation
DNAdam↑,
Bcl-2↓, Mechanistically, APS downregulate antiapoptotic proteins such as Bcl-2 while upregulating proapoptotic proteins such as Bax and cleaved caspase-3.
BAX↑,
MMP↓, APS have been shown to disrupt the mitochondrial membrane potential and promote the release of cytochrome c, thereby enhancing apoptotic cascades in hepatocellular carcinoma models.
Cyt‑c↑,
NOTCH1↓, APS (0.1, 0.5, and 1.0 mg/mL) were shown to reduce both mRNA and protein levels of Notch1 in a concentration-dependent manner.
GSK‐3β↓, APS significantly inhibited the proliferation of HepG2 cells by downregulating the expression of glycogen synthase kinase-3β (GSK-3β), with 200 μg/mL being the most effective concentration.
TumCCA↑, APS exerted these effects by inducing cell cycle arrest at the G2/M and S phases, thereby impeding tumour cell proliferation [35].
GSH↓, HepG2 cells. APS also reduced intracellular glutathione (GSH) levels, increased reactive oxygen species (ROS) and lipid peroxidation levels, and elevated intracellular iron ion concentrations—all in a dose-dependent manner.
ROS↑,
lipid-P↑,
c-Iron↑,
GPx4↓, APS treatment led to the downregulation of GPX4 and upregulation of ACSL4, indicating that APS promotes ferroptosis in liver cancer cells.
ACSL4↑,
Ferroptosis↑,
Wnt↓, inhibit the expression of key proteins involved in the Wnt/β-catenin signalling pathway
β-catenin/ZEB1↓,
cycD1/CCND1↓, by downregulating the key oncogenic targets, including β-catenin, C-myc, and cyclin D1, which subsequently reduces Bcl-2 expression and activates the apoptotic cascade in HepG2 liver cancer cells.
Akt↓, It also inhibited the Akt/p-Akt signalling pathway.
PI3K↓, APS inhibit the PI3K/AKT/mTOR signalling pathway, which is a central negative regulator of autophagy.
mTOR↓,
CXCR4↓, PS upregulated the epithelial marker E-cadherin while downregulating the mesenchymal marker vimentin and the chemokine receptor CXCR4 at both mRNA and protein levels, suggesting that APS suppress liver cancer cell growth and metastasis by inhibiting
Vim↓,
PD-L1↓, APS interfere with immune checkpoint signalling by downregulating Programmed death-ligand 1 (PD-L1) expression on tumour cells.
eff↑, The preparation of polysaccharide–SeNP composites typically involves using sodium selenite (Na2SeO3) as the precursor and ascorbic acid (Vc) as the reducing agent, with synthesis carried out via a chemical reduction method in a polysaccharide solutio
eff↑, Mechanistic investigations revealed that AASP–SeNPs elevated intracellular ROS levels and reduced the mitochondrial membrane potential (∆Ψm).
ChemoSen↑, APS enhance doxorubicin-induced endoplasmic reticulum (ER) stress by reducing O-GlcNAcylation levels, thereby promoting apoptosis of liver cancer cells.
ChemoSen↑, APS inhibited BEL-7404 human liver cancer cell growth in a concentration-dependent manner and showed stronger cytotoxicity when combined with cisplatin.
chemoP↑, APS protects against chemotherapy-induced liver injury, particularly that caused by CTX, through antiapoptotic mechanisms
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↓,
TumCP↓, BSS-SNPs significantly inhibited the proliferation and induced ROS and Nrf-2 expression in HepG2 cells.
ROS↑,
NRF2↑,
BAX↑, BSS-SNPs treatment caused apoptosis-related morphological changes and upregulated the pro-apoptotic markers such as bax, p53, cytochrome c, and caspases-9, -3 and downregulated bcl-2 expressions.
P53↑,
Cyt‑c↑,
Casp9↑,
Casp3↑,
Bcl-2↓,
TrxR↓, Exposure likewise inhibited TrxR activity in cultured cells, and Ag ions were potent inhibitors of purified rat TrxR isoform 1 (cytosolic) (TrxR1) enzyme.
TrxR1↓, Exposure to AgNPs leads to the inhibition of selenoprotein synthesis and inhibition of TrxR1
ROS↑, likely mechanism underlying increases in oxidative stress
ER Stress↑, increases endoplasmic reticulum stress,
TumCP↓, reduced cell proliferation during exposure to Ag.
selenoP↓, Exposure to AgNPs inhibits incorporation of selenium into selenoproteins.
TNF-α↓, AgNPs-CIT inhibited TNFα expression via deactivation of the NF-κB signaling event
NF-kB↓,
antiOx↑, best antioxidant activity of AgNPs-CIT was found at >40% (~ 42%) radicals inhibitions at 10 mg/mL concentration
TumCP↓, cancer cell proliferation was significantly decreased when pretreated with AgNPs-CIT for 2 h and then stimulated with PMA for 24 h
ROS↑, This review focus on the abilities of nanoparticles to induce oxidative stress, prevent proliferation, and trigger apoptosis in cancer cells.
TumCP↓,
Apoptosis↑,
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Pca, |
PC3 |
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in-vitro, |
Pca, |
LNCaP |
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in-vitro, |
Pca, |
DU145 |
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selectivity↑, Both AgNPs and G-AgNPs were cytotoxic only to CRPC cells and not to hormone-sensitive ones and their effect was higher after functionalization showing the potential of glucose to favor AgNPs’ uptake by cancer cells.
ROS↑, NPs increased the ROS, inducing mitochondrial damage, and arresting cell cycle in S Phase, therefore blocking proliferation, and inducing apoptosis.
mtDam↑,
TumCCA↑,
TumCP↓,
Apoptosis↑,
MMP↓, AgNPs were able to depolarize the cells’ mitochondria to 32.74% and 10.36%, respectively
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in-vitro, |
Kidney, |
786-O |
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ROS↑, AgNPs are cytotoxic to 786-O cells, a ccRCC cell line, entering through endocytosis, increasing ROS, depolarizing mitochondrial membrane, and blocking the cell cycle, leading to a reduction of proliferation capacity and apoptosis.
MMP↑,
TumCCA↑,
TumCP↓,
Apoptosis↑,
RadioS↑, 786-O is intrinsically resistant to radiation, but after AgNPs’ administration, radiation induces cytotoxicity through mitochondrial membrane depolarization and S phase blockage.
TumCP↓, anti-proliferative and cytotoxic studies in KB oral cancer cells
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Review, |
Var, |
NA |
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Review, |
Diabetic, |
NA |
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ROS↑, action mechanisms of AgNPs, which mainly involve the release of silver ions (Ag+), generation of reactive oxygen species (ROS), destruction of membrane structure.
eff↑, briefly introduce a new type of Ag particles smaller than AgNPs, silver Ångstrom (Å, 1 Å = 0.1 nm) particles (AgÅPs), which exhibit better biological activity and lower toxicity compared with AgNPs.
other↝, This method involves reducing silver ions to silver atoms 9, and the process can be divided into two steps, nucleation and growth
DNAdam↑, antimicrobial mechanisms of AgNPs includes destructing bacterial cell walls, producing reactive oxygen species (ROS) and damaging DNA structure
EPR↑, Due to the enhanced permeability and retention (EPR) effect, tumor cells preferentially absorb NPs-sized bodies than normal tissues
eff↑, Large surface area may lead to increased silver ions (Ag+) released from AgNPs, which may enhance the toxicity of nanoparticles.
eff↑, Our team prepared Ångstrom silver particles, capped with fructose as stabilizer, can be stable for a long time
TumMeta↓, AgNPs can induce tumor cell apoptosis through inactivating proteins and regulating signaling pathways, or blocking tumor cell metastasis by inhibiting angiogenesis
angioG↓, Various studies support that AgNPs can deprive cancer cells of both nutrients and oxygen via inhibiting angiogenesis
*Bacteria↓, Rather than Gram-positive bacteria, AgNPs show a stronger effect on the Gram-negative ones. This may be due to the different thickness of cell wall between two kinds of bacteria
*eff↑, In general, as particle size decreases, the antibacterial effect of AgNPs increases significantly
*AntiViral↑, AgNPs with less than 10 nm size exhibit good antiviral activity 185, 186, which may be due to their large reaction area and strong adhesion to the virus surface.
*AntiFungal↑, Some studies confirm that AgNPs exhibit good antifungal properties against Colletotrichum coccodes, Monilinia sp. 178, Candida spp.
eff↑, The greater cytotoxicity and more ROS production are observed in tumor cells exposed to high positive charged AgNPs
eff↑, Nanoparticles exposed to a protein-containing medium are covered with a layer of mixed protein called protein corona. formation of protein coronas around AgNPs can be a prerequisite for their cytotoxicity
TumCP↓, Numerous experiments in vitro and in vivo have proved that AgNPs can decrease the proliferation and viability of cancer cells.
tumCV↓,
P53↝, gNPs can promote apoptosis by up- or down-regulating expression of key genes, such as p53 242, and regulating essential signaling pathways, such as hypoxia-inducible factor (HIF) pathway
HIF-1↓, Yang et al. found that AgNPs could disrupt the HIF signaling pathway by attenuating HIF-1 protein accumulation and downstream target genes expression
TumCCA↑, Cancer cells treated with AgNPs may also show cell cycle arrest 160, 244
lipid-P↑, Ag+ released by AgNPs induces oxidation of glutathione, and increases lipid peroxidation in cellular membranes, resulting in cytoplasmic constituents leaking from damaged cells
ATP↓, mitochondrial function can be inhibited by AgNPs via disrupting mitochondrial respiratory chain, suppressing ATP production
Cyt‑c↑, and the release of Cyt c, destroy the electron transport chain, and impair mitochondrial function
MMPs↓, AgNPs can also inhibit the progression of tumors by inhibiting MMPs activity.
PI3K↓, Various studies support that AgNPs can deprive cancer cells of both nutrients and oxygen via inhibiting angiogenesis
Akt↓,
*Wound Healing↑, AgNPs exhibit good properties in promoting wound repair and bone healing, as well as inhibition of inflammation.
*Inflam↓,
*Bone Healing↑,
*glucose↓, blood glucose level of diabetic rats decreased when treated with AgNPs for 14 days and 21 days without significant acute toxicity.
*AntiDiabetic↑,
*BBB↑, The small-sized AgNPs are easy to penetrate the body and cross biological barriers like the blood-brain barrier and the blood-testis barrier
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vitro+vivo, |
Bladder, |
5637 |
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TumCD↑, 57% tumor regression
Apoptosis↑,
TumCMig↓,
TumCP↓,
TumCP↓, especially in the G0/G1 and S phases.
Casp3↑,
P53↑,
Beclin-1↑,
TumAuto↑,
GSR↑, oxidative stress biomarker
ROS↑, oxidative stress biomarker
MDA↑, oxidative stress biomarker
ROS↑,
SIRT1↑,
Ca+2↑, induce apoptosis in osteoclasts by increasing intracellular and nucleus Ca2+ concentration
Endon↑, increases endonuclease activity
DNAdam↑,
Apoptosis↑,
NF-kB↓,
Ki-67↓,
TumCP↓,
CD34↓,
BAX↑,
*TumCP↓, AgNPs affects the morphology and function of endothelial cells which manifests as decreased cell proliferation, migration, and angiogenesis ability
*ROS↑, AgNPs can induce excessive cellular production of reactive oxygen species (ROS), leading to damage to cellular sub-organs such as mitochondria and lysosomes
*eff↓, treatment with ROS scavenger-NAC can effectively suppress AgNP-induced endothelial damage.
*MDA↑, exposure to AgNPs increased MDA levels and decreased GSH levels.
*GSH↓,
*MMP↓, significantly reduced both MMP and ATP levels (Fig. 7) in HUVECs,
*ATP↓,
*LC3II↑, expression levels of LC3-II and p62 were significantly increase
*p62↑,
*Bcl-2↓, the anti-apoptotic protein expression level of Bcl-2 in HUVECs decreased, while the pro-apoptotic protein expression levels of Bax and Caspase-3 increased significantly.
*BAX↑,
*Casp3↑,
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NA |
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vitro+vivo, |
NA, |
NA |
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ROS↑, This study introduces zinc oxide (ZnO) nanorods (NRs) in situ loaded with silver nanoparticles (ZnO@Ag NRs), designed to optimize ROS production under ultrasound irradiation and offer significant advantages in tumor specificity and biosafety
eff↑, In conclusion, our findings confirmed that the ROS production ability of ZnO@Ag exceeded that of ZnO and is highly depended on the duration of US treatment in this study.
eff↑, The ZnO@Ag group had the most effective cell-killing effects under ultrasound (1.5 W/cm2, 50% duty cycle, 1 MHz, 5 min) than any of the other five groups
TumCP↓, ZnO@Ag significantly inhibited tumor cell proliferation, consistent with earlier tumor growth curve findings
toxicity↓, None of the intervention groups showed significant organ toxicity
eff↑, Ajoene (4,5,9-trithiadodeca-1,6,11-triene-9-oxide) is a garlic-derived compound produced most efficiently from pure allicin and has the advantage of a greater chemical stability than allicin.
AntiThr↑, ajoene have demonstrated its best-known anti-thrombosis, anti-microbial and cholesterol lowering activities.
Bacteria↓,
LDH↓,
TumCP↓, Ajoene was shown to inhibit proliferation and induce apoptosis of several human leukaemia CD34-negative cells including HL-60, U937, HEL and OCIM-1
TumCCA↑, Studies have shown the anti-proliferation activity of ajoene to be associated with a block in the G2/M phase of cell cycle in human myeloid leukaemia cells.
Bcl-2↓, The apoptosis inducing activity of ajoene is via the mitochondria-dependent caspase cascade through a significant reduction of the anti-apoptotic bcl-2 that results in release of cytochrome c and the activation of caspase-3.
Cyt‑c↑,
Casp3↑,
*cardioP↑, Allicin has many health-promoting properties, such as cardioprotective, antimicrobic, cholesterol-lowering, anti-inflammatory, and antitumor.
*Bacteria↓,
*Inflam↓,
AntiTum↑,
*DNAdam↓, DNA damage protection, induction of cell death, inhibition of cell proliferation, and block of angiogenesis and metastasis formation.
TumCP↓,
angioG↓,
TumMeta↓,
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
| - |
vitro+vivo, |
ESCC, |
TE1 |
|
|
|
- |
vitro+vivo, |
ESCC, |
KYSE-510 |
|
|
|
- |
in-vitro, |
Nor, |
Het-1A |
|
|
|
TumCP↓,
LC3‑Ⅱ/LC3‑Ⅰ↑,
p62↓,
p‑AMPK↑,
mTOR↓,
TumAuto↑,
NCOA4↑,
MDA↑,
Iron↑, elevated malondialdehyde and Fe2+ production levels
TumW↓,
TumVol↓,
ATG5↑,
ATG7↑,
TfR1/CD71↓,
FTH1↓, suppressed the expression of ferritin heavy chain 1 (the major intracellular iron-storage protein)
ROS↑,
Iron↑,
Ferroptosis↑,
*toxicity↓, 80 μg/mL allicin for 24 h did not change the viability of Het-1A cells. A slight reduction in cell viability was observed when Het-1A cells were treated with 160 μg/mL allicin for 24 h
| - |
in-vitro, |
Nor, |
3T3 |
|
|
|
- |
in-vitro, |
BC, |
MCF7 |
|
|
|
- |
in-vitro, |
Lung, |
A549 |
|
|
|
- |
in-vitro, |
CRC, |
HT-29 |
|
|
|
Thiols↓, Garlic produces the thiol-reactive defence substance, allicin, upon wounding.
tumCV↓, Allicin reduced cell viability and cell proliferation in a concentration dependent manner.
TumCP↓, Allicin Inhibits Cell Proliferation
GSH↓, allicin reacts with and depletes the GSH pool.
GSSG↑, Allicin is a thiol-reagent and reacts easily with glutathione, forming S-allylmercaptoglutathione (GSSA) and leading to an increased production of GSSG
ROS↑, Allicin oxidizes thiols and causes oxidative stress in its own right.
| - |
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↑,
| - |
in-vitro, |
BC, |
MCF7 |
|
|
|
- |
in-vitro, |
BC, |
MDA-MB-231 |
|
|
|
TumCP↓,
Akt↓,
ERK↓,
IGF-1R↓,
Furin↓,
Ki-67↓,
AMPK↑,
mTOR↓,
| - |
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
| - |
vitro+vivo, |
Ovarian, |
NA |
|
|
|
antiNeop↑, We have recently demonstrated the anti-neoplastic effect of Amla extract (Emblica officinalis, AE) on OC cells in vitro and in vivo.
TumCP↓, The inhibitory effect of AE on proliferation, migration and invasiveness (P≤0.001) of SKOV3 cells and >90% attenuation of tumor growth in a xenograft mouse model suggested multiple targets.
TumCMig↓,
TumCI↓,
TumCG↓,
miR-375↑, >2,000-fold increase in the expression of miR-375 in AE-treated SKOV3 cells
IGFR↓, AE also decreased the gene and protein expression of IGF1R, a target of miR-375 (P≤0.001), and SNAIL1 (P≤0.002), an EMT-associated transcription factor that represses E-cadherin expression (P≤0.003).
Snail↓,
E-cadherin↑, AE increased E-cadherin expression (P≤0.001).
| - |
vitro+vivo, |
Ovarian, |
OVCAR-3 |
|
|
|
- |
in-vitro, |
Ovarian, |
SW626 |
|
|
|
TumCP↓, Amla extract (AE) has anti-proliferative effects on OC cells under both in vitro and in vivo conditions.
Beclin-1↑, AE did not induce apoptotic cell death, but did significantly increase the expression of the autophagic proteins beclin1 and LC3B-II under in vitro conditions.
LC3B-II↑,
Hif1a↓, AE also significantly reduced the expression of several angiogenic genes, including hypoxia-inducible factor 1α (HIF-1α) in OVCAR3 cells.
Dose↝, cell proliferation was significantly inhibited at AE concentrations ranging from 300–1000 µg/ml
TumAuto↑, AE induces autophagy in OVCAR3 and SW626 cells
angioG↓, AE inhibits angiogenesis-related genes in OVCAR3 cells
COL4A3↓, The expression of COL4A3, CXCL6, ECGF1, EFNB2, FGF2, IL1β, PDGFB, TNFRSF12A and HIF-1α were reduced to less than 40% of control levels (Figure 5D), with Hif-1α being inhibited to the greatest extent.
CXCL6/GCP-2↓,
TYMP/ECGF1↓,
IL1β↓,
PDGFRB↓,
ChemoSen↑, AE with cisplatin synergistically reduced cell proliferation in OVCAR3 cells
Dose↝, mice were fed orally with 10% sucrose (control) or 10% sucrose with AE (100 mg/kg body wt.) daily.
| - |
in-vitro, |
BC, |
HCC1806/CRL-2335 |
|
|
|
- |
in-vitro, |
BC, |
MDA-MB-231 |
|
|
|
- |
in-vitro, |
BC, |
MDA-MB-468 |
|
|
|
TumCP↓, We found that DTS inhibits proliferation and migration of CRL-2335 cells derived from a patient of West African ancestry.
TumCMig↓,
Bak↑, DTS induces the expression of pro-apoptotic genes BAK1, GADD45a, and LTA in CRL2335 cells though it primarily promotes caspase-independent CRL-2335 cell death.
GADD45A↑,
LTA/TNF-β↑, Finally, Kaplan-Meier survival curves reveal that higher expression of BAK1 and LTA in tumors from patients with TNBC is associated with longer relapse-free survival.
lysoMP↑, DTS promotes lysosomal membrane permeabilization and cathepsin B release in CRL2335 cells
P450↓, We previously found that DTS suppressed cytochrome P450 1 (CYP1) activity and binds to the CYP1A1 active site
cl‑PARP↑, DTS induces PARP in a dose-dependent manner (Figure 7) and cleaved PARP is expressed more robustly than cleaved caspase 3.
Dose↝, it is recommended that patients use P. alliacea twice daily for an extended period [67], to allow sufficient levels to accumulate in the plasma.
| - |
vitro+vivo, |
NSCLC, |
H1299 |
|
|
|
- |
in-vitro, |
NSCLC, |
A549 |
|
|
|
TumCP↓, DTS significantly inhibited H1299 and A549 cells proliferation, migration, invasion, and induced cell apoptosis in vitro.
TumCMig↓,
TumCI↓,
Apoptosis↑,
BAX↑, DTS induced the expression of the pro-apoptotic gene Bax and reduced the expression of the anti-apoptotic gene Bcl-2.
Bcl-2↓,
EMT↓, DTS attenuated epithelial-mesenchymal transition (EMT), which was associated with inhibition of STAT3 phosphorylation.
p‑STAT3↓,
TumCG↓, DTS dose-dependently suppressed the tumor growth in H1299 xenograft mice.
AntiTum↑, We previously demonstrated that the alcoholic extract of Petiveria alliacea (Esperanza) has a significant in vitro antitumor effect on other tumor cells and also the ability to regulate energy metabolism.
GlucoseCon↓, extract modulates tumor metabolism by decreasing glucose uptake and increasing reactive oxygen species, which leads to a reduction in cell proliferation.
ROS↑,
TumCP↓,
eff↓, The Esperanza extract does not present a marked cytotoxic activity in any of the cell lines evaluated (DA-3/ER-GM, U937, MCF-7, MDA-MB-468 and 3T3), except on 4T1, where the IC50 is less than 50 µg/mL
Glycolysis↓, One of the major compounds found in Esperanza was citric acid. This is one of the most effective inhibitors of glycolysis, which inhibits the phosphofructokinase enzyme blocking glycolysis at the start;
| - |
in-vitro, |
HNSCC, |
HN30 |
|
|
|
- |
in-vitro, |
Tong, |
SCC25 |
|
|
|
tumCV↓, DTS dose-dependently decreased HN30 cell viability as compared with the solvent control group, and 100 μmol/L DTS produced the strongest inhibitory effect (P < 0.0001).
Apoptosis↑, Treatment with DTS below 30 μmol/L concentrationdependently promoted apoptosis (P < 0.01) and lowered the MMP (P < 0.01) of HN30 cells
MMP↓,
cl‑Casp3↑, the cells showed significantly increased cleaved caspase-3 (P < 0.01) and decreased Bcl-2 expression (P < 0.01).
Bcl-2↓,
p‑Akt↓, Treatment with 10 μmol/L DTS for 16 h significantly inhibited Akt phosphorylation
p‑P53↑, enhanced p53 phosphorylation (P < 0.01) in HN30 cells.
TumCP↓, DTS inhibits proliferation and induces apoptosis of HN30 cells possibly through mechanisms involving the inhibition of Akt and the activation of p53.
TumCP↓, P. alliacea reduces K562 cell proliferation
OCR↓, P. Alliacea extract decreased the oxygen consumption rate and intracellular ATP.
ATP↓,
TumCCA↑, leading to cell cycle arrest.
ECAR↑, Esperanza extract induced a significant reduction in the OCR (Figure 4A) and a slight increase in the ECAR
Glycolysis↓, P. alliacea induces changes in the cellular expression of several glycolytic enzymes, a decrease in glycolysis, lactate production, and mitochondrial respiration, and a reduction in β-F1-ATPase, ultimately leading to ATP deficiency
lactateProd↓,
mitResp↓,
TumCP↓,
TumCCA↑,
Apoptosis↑,
STAT3↓,
Akt↓,
P21↑,
BAX↑,
cycD1/CCND1↓,
cycE/CCNE↓,
survivin↓,
XIAP↓,
Bcl-2↓,
eff↑, ANDRO combined with gemcitabine significantly induce stronger cell cycle arrest and more obvious apoptosis than each single treatment.
| - |
in-vitro, |
PC, |
NA |
|
|
|
- |
in-vivo, |
PC, |
NA |
|
|
|
Apoptosis↑,
DJ-1↓, reduction in DJ-1 expression caused by Andro led to ROS accumulation
ROS↑,
TumAuto↑,
TumCCA↑, G2/M phase
TumCP↓,
TumW↓,
eff↓, pro-apoptotic effect of Andro was attenuated when NAC was co-administered
| - |
in-vitro, |
BC, |
MDA-MB-231 |
|
|
|
- |
in-vitro, |
Nor, |
HUVECs |
|
|
|
- |
in-vivo, |
BC, |
MCF7 |
|
|
|
- |
in-vitro, |
BC, |
T47D |
|
|
|
- |
in-vitro, |
BC, |
BT549 |
|
|
|
- |
in-vitro, |
BC, |
MDA-MB-361 |
|
|
|
TumCP↓,
COX2/PTGS2↓, suppress COX-2 expression at both protein and mRNA levels.
*angioG↓,
Cyt‑c↑,
CREB2↓, inhibited the binding of the transactivators CREB2, C-Fos and NF-κB
cFos↓,
NF-kB↓,
HATs↓,
cl‑Casp3↑,
cl‑Casp9↑,
Bax:Bcl2↑,
Apoptosis↑,
*toxicity↓, IC50: 50uM for normal vs 20-35uM for cancer cells
AntiCan↑, Anethole, a bioactive compound found in essential oils of anise and fennel, commonly used as a food preservative, has recently garnered attention for its potential anti-cancer properties.
Apoptosis↑, Anethole demonstrates multiple anti-cancer mechanisms, such as inducing apoptosis, causing cell cycle arrest, exhibiting anti-proliferative and anti-angiogenic effects, and modulating critical signaling pathways including NF-κB, PI3K/Akt/mTOR, and ca
TumCCA↑,
TumCP↓,
angioG↓,
NF-kB↓,
PI3K↓,
Akt↓,
mTOR↓,
Casp↓,
ChemoSen↑, It enhances the efficacy of chemotherapeutic agents like cisplatin and doxorubicin while reducing their toxicity
| - |
in-vitro, |
BC, |
MCF7 |
|
|
|
- |
in-vitro, |
BC, |
MDA-MB-231 |
|
|
|
Apoptosis↑, anethole may be viable as an anti-cancer agent through the modulation of apoptosis, cell survival and proliferation in breast cancer cells
tumCV↓,
TumCP↓,
TumCP↓, anethole inhibited proliferation, clonal growth and migration of PC-3 cells.
TumCG↓,
TumCMig↓,
CSCs↓, It also suppressed growth of PC-3 derived cancer stem cells (tumorspheres).
ROS↑, Pro-apoptotic potential of anethole was accompanied by generation of ROS, permeabilization of the mitochondrial and lysosomal membranes, activation of caspase-3 and -9, DNA damage, PARP cleavage and induction of Bax/Bcl-2 protein ratio.
MPT↑,
Casp3↑,
Casp9↑,
DNAdam↑,
cl‑PARP↑,
Bax:Bcl2↑,
TumCCA↑, anethole induced G2/M phase arrest, downregulation of cyclins D1, CDK-4 and c-Myc proteins and upregulation of p21 and p27.
cycD1/CCND1↓,
CDK4↓,
cMyc↓,
P21↑,
p27/CDKN1B↑,
NF-kB↓, Anethole suppressed nuclear localization of NF-κB protein and downregulated transcription of NF-κB-dependent genes.
eff↑, the above findings highlight the effectiveness of anethole as a potential candidate for prostate cancer therapy.
AntiCan↑, anethole possesses an anti-oral cancer effect
ChemoSen↑, anethole (3 µM) potentiates cisplatin-induced inhibition of cell proliferation and decreases the ΔΨm on Ca9-22 cells.
TumCP↓,
MMP↓,
ROS↑, we also found anethole and cisplatin to enhance the cisplatin-induced generation of reactive oxygen species (ROS) and mitochondrial stress.
MAPK↓, inhibited by the combination of anethole and cisplatin such as MAPKase, beta-catenin, and NF-κB pathways.
β-catenin/ZEB1↓,
NF-kB↓,
EMT↓, anethole potentiates the effect of cisplatin against oral cell migration by blocking the epithelial-to-mesenchymal transition.
Casp↑, Anethole Synergy with Cisplatin in the Induction of Apoptosis via Caspase Activation
| - |
vitro+vivo, |
NSCLC, |
A549 |
|
|
|
TumCP↓, Anethole inhibited proliferation and clonal growth of A549 cells.
TumCG↓,
Apoptosis↑, The promotion of A549 cell apoptosis by anethole was evidenced by increased apoptotic ratio, abundant DNA fragments, and caspase-3 activation.
DNAdam↑,
Casp3↑,
PI3K↓, PI3K-AKT and STAT3 signaling pathways were decreased in anethole group.
Akt↓,
STAT3↓,
Ki-67↓, xenografted tumors in anethole group retarded with decreased Ki67 and increased cleaved caspase 3 expression.
cl‑Casp3↑,
Showing Research Papers: 1 to 50 of 994
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* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 994
Pathway results for Effect on Cancer / Diseased Cells:
NA, unassigned(tgid=0) ⓘ
COL4A3↓, 1, CXCL6/GCP-2↓, 1, miR-375↑, 1, TYMP/ECGF1↓, 1,
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↑, 1, DJ-1↓, 1, Ferroptosis↑, 2, GPx4↓, 2, GSH↓, 2, GSR↑, 1, GSSG↑, 1, Iron↑, 2, c-Iron↑, 1, lipid-P↑, 2, MDA↑, 2, NRF2↑, 1, OXPHOS↓, 1, ROS↑, 21, selenoP↓, 1, Thiols↓, 1, TrxR↓, 3, TrxR1↓, 1, xCT/SLC7A11↓, 1,
Metal & Cofactor Biology(tgid=2) ⓘ
FTH1↓, 1, NCOA4↑, 1, TfR1/CD71↓, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
AIF↑, 2, ATP↓, 4, mitResp↓, 1, MMP↓, 7, MMP↑, 1, MPT↑, 2, mtDam↑, 1, OCR↓, 1, XIAP↓, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
ACSL4↑, 1, AMPK↑, 5, p‑AMPK↑, 1, ATG7↑, 1, cMyc↓, 1, ECAR↑, 1, FDG↓, 1, GlucoseCon↓, 1, Glycolysis↓, 4, H2S↑, 1, HK2↓, 1, lactateProd↓, 1, LDH↓, 2, PDH↓, 1, PDH↑, 1, SIRT1↓, 1, SIRT1↑, 1, SREBP1/SREBF1↓, 1,
Cell Death(tgid=5) ⓘ
Akt↓, 12, p‑Akt↓, 1, Apoptosis↓, 1, Apoptosis↑, 23, Bak↑, 1, BAX↑, 7, Bax:Bcl2↑, 2, Bcl-2↓, 8, Bcl-xL↓, 1, Casp↓, 1, Casp↑, 3, Casp3↑, 7, cl‑Casp3↑, 4, Casp8↑, 1, Casp9↑, 3, cl‑Casp9↑, 1, Cyt‑c↑, 6, Endon↑, 1, Fas↓, 1, Fas↑, 2, FasL↓, 1, Ferroptosis↑, 2, JNK↓, 2, lysoMP↑, 1, MAPK↓, 2, p27/CDKN1B↑, 1, p38↑, 1, survivin↓, 2, TumCD↑, 2,
Transcription & Epigenetics(tgid=7) ⓘ
AntiThr↑, 1, HATs↓, 1, other↓, 1, other↝, 1, tumCV↓, 4,
Protein Folding & ER Stress(tgid=8) ⓘ
ER Stress↑, 2,
Autophagy & Lysosomes(tgid=9) ⓘ
ATG5↑, 1, Beclin-1↑, 3, LC3‑Ⅱ/LC3‑Ⅰ↑, 1, LC3B-II↑, 1, p62↓, 1, TumAuto↑, 5,
DNA Damage & Repair(tgid=10) ⓘ
DNAdam↑, 7, GADD45A↑, 1, P53↑, 3, P53↝, 1, p‑P53↑, 2, cl‑PARP↑, 4,
Cell Cycle & Senescence(tgid=11) ⓘ
CDK4↓, 2, CycB/CCNB1↑, 1, cycD1/CCND1↓, 6, cycE/CCNE↓, 2, P21↑, 4, TumCCA↑, 12,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
CD133↓, 1, CD34↓, 1, CD44↓, 1, cFos↓, 1, CREB2↓, 1, CSCs↓, 3, EMT↓, 8, ERK↓, 1, GSK‐3β↓, 2, IGF-1R↓, 1, IGFR↓, 1, mTOR↓, 8, NOTCH1↓, 3, NOTCH3↓, 1, PDGFRB↓, 1, PI3K↓, 8, STAT3↓, 2, p‑STAT3↓, 1, TOP1↓, 1, TOP2↓, 1, TumCG↓, 12, Wnt↓, 3,
Migration(tgid=13) ⓘ
Ca+2↑, 2, E-cadherin↑, 5, Furin↓, 1, Ki-67↓, 4, miR-133a-3p↑, 1, MMP2↓, 1, MMP9↓, 3, MMPs↓, 1, N-cadherin↓, 2, p‑SMAD2↓, 1, Snail↓, 3, TGF-β↓, 2, TGF-β1↓, 1, TumCI↓, 8, TumCMig↓, 11, TumCP↓, 49, TumMeta↓, 3, Twist↓, 1, Vim↓, 4, β-catenin/ZEB1↓, 5,
Angiogenesis & Vasculature(tgid=14) ⓘ
angioG↓, 5, EGFR↓, 2, EGR4↓, 1, EPR↑, 1, HIF-1↓, 2, Hif1a↓, 2, VEGF↓, 2,
Barriers & Transport(tgid=15) ⓘ
P-gp/ABCB1↓, 2,
Immune & Inflammatory Signaling(tgid=16) ⓘ
COX2/PTGS2↓, 1, CXCR4↓, 1, IL12↑, 1, IL1β↓, 1, IL2↑, 1, IL6↓, 1, Imm↑, 2, Inflam↓, 1, LTA/TNF-β↑, 1, NF-kB↓, 11, NF-kB↑, 1, p50↓, 1, PD-L1↓, 1, TNF-α↓, 2, TNF-α↑, 1,
Hormonal & Nuclear Receptors(tgid=20) ⓘ
CDK6↓, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↓, 1, BioAv↑, 1, BioAv↝, 1, ChemoSen↑, 11, Dose↝, 5, eff↓, 3, eff↑, 20, eff↝, 1, Half-Life↓, 1, MDR1↓, 1, P450↓, 1, RadioS↑, 2, selectivity↑, 3,
Clinical Biomarkers(tgid=22) ⓘ
EGFR↓, 2, IL6↓, 1, Ki-67↓, 4, LDH↓, 2, PD-L1↓, 1,
Functional Outcomes(tgid=23) ⓘ
AntiCan↑, 5, antiNeop↑, 1, AntiTum↑, 4, chemoP↑, 2, QoL↑, 2, toxicity↓, 2, TumVol↓, 2, TumW↓, 2,
Infection & Microbiome(tgid=24) ⓘ
Bacteria↓, 1,
Total Targets: 199
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↑, 2, GSH↓, 1, GSH↑, 1, lipid-P↓, 1, MDA↑, 1, NRF2↑, 1, ROS↓, 1, ROS↑, 1,
Metal & Cofactor Biology(tgid=2) ⓘ
IronCh↑, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
ATP↓, 1, MMP↓, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
glucose↓, 1, GlucoseCon↑, 1,
Cell Death(tgid=5) ⓘ
BAX↑, 1, Bcl-2↓, 1, Casp3↑, 1,
Transcription & Epigenetics(tgid=7) ⓘ
Ach↑, 1, other↓, 1, other↝, 1,
Autophagy & Lysosomes(tgid=9) ⓘ
LC3II↑, 1, p62↑, 1,
DNA Damage & Repair(tgid=10) ⓘ
DNAdam↓, 1,
Migration(tgid=13) ⓘ
TumCP↓, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
angioG↓, 1,
Barriers & Transport(tgid=15) ⓘ
BBB↑, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
IL1β↓, 1, IL6↓, 1, Imm↑, 1, Inflam↓, 3,
Synaptic & Neurotransmission(tgid=18) ⓘ
ChAT↑, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↑, 2, BioAv↝, 1, eff↓, 1, eff↑, 1, Half-Life↓, 1,
Clinical Biomarkers(tgid=22) ⓘ
GutMicro↑, 1, IL6↓, 1,
Functional Outcomes(tgid=23) ⓘ
AntiDiabetic↑, 1, Bone Healing↑, 1, cardioP↑, 1, chemoP↑, 1, memory↑, 1, neuroP↑, 1, toxicity↓, 2, Wound Healing↑, 1,
Infection & Microbiome(tgid=24) ⓘ
AntiFungal↑, 1, AntiViral↑, 1, Bacteria↓, 2,
Total Targets: 48
Scientific Paper Hit Count for: TumCP, Tumor Cell proliferation
44
Curcumin24
Thymoquinone23
Quercetin23
Shikonin18
EGCG (Epigallocatechin Gallate)18
Resveratrol18
Sulforaphane (mainly Broccoli)17
Magnetic Fields16
Baicalein16
Berberine14
Silver-NanoParticles14
Apigenin (mainly Parsley)14
IP6 (Inositol 1,2,3,4,5,6-hexakisphosphate)14
Phenethyl isothiocyanate13
Formononetin12
Capsaicin12
Fisetin12
Garcinol12
Honokiol12
Propolis -bee glue11
Artemisinin11
Ashwagandha(Withaferin A)11
Radiotherapy/Radiation11
Boron11
Crocetin11
Emodin11
Nimbolide10
Metformin10
Magnolol10
Lycopene10
Silymarin (Milk Thistle) silibinin10
Urolithin9
Cisplatin9
Astaxanthin9
Berbamine9
Chrysin9
Gallic acid9
Hyperoside9
Luteolin9
Selenite (Sodium)8
Citric Acid8
chitosan8
chaetocin8
Dandelion Root8
HydroxyTyrosol8
Isobavachalcone7
Astragalus7
Anethole/trans-Anethole7
Beta-Caryophyllene7
Bufalin/Huachansu7
Centella asiatica / Gotu kola → asiaticoside7
Eugenol7
Ferulic acid7
Gambogic Acid7
Ginkgetin7
isoorientin7
Piperlongumine6
Boswellia (frankincense)6
Chemotherapy6
Carnosic acid6
Rosmarinic acid6
Celastrol6
Carvone6
Cucurbitacin6
Diclofenac6
Ellagic acid6
Evodiamine6
Isoliquiritigenin6
salinomycin5
DTS(dibenzyl trisulphide) from Anamu5
Gemcitabine (Gemzar)5
Betulinic acid5
Carvacrol5
Cinnamon5
5-fluorouracil5
Deguelin5
D-limonene5
Fucoidan5
Galloflavin5
Geraniol5
Hydrogen Gas5
Helleborus niger extracts – Christmas Rose5
Juglone5
Phenylbutyrate5
Vitamin K24
Allicin (mainly Garlic)4
Melatonin4
Paclitaxel/Taxol4
Atorvastatin4
brusatol4
Celecoxib4
Chlorogenic acid4
Chlorophyllin4
Photodynamic Therapy4
Date Fruit Extract4
Genistein (soy isoflavone)4
Fenbendazole4
Ginger/6-Shogaol/Gingerol4
Indole-3-carbinol4
iodine4
Inositol4
isoquercitrin4
Magnetic Field Rotating4
Piperine4
Ursolic acid3
1,8-Cineole3
Alpha-Lipoic-Acid3
Andrographis3
Isovitexin3
Aspirin3
immunotherapy3
Docetaxel3
α-Bisabolol / Chamomile oil3
Caffeic acid3
Thymol-Thymus vulgaris3
Chocolate3
Cichoric acid / Chicoric acid3
Cyclopamine3
Cynaropicrin3
Dichloroacetate3
diet Methionine-Restricted Diet3
Disulfiram3
Copper and Cu NanoParticles3
Ginkgo biloba-EGb 7613
Ginkgo biloba3
Ginkgolide B3
Linalool3
Methylene blue3
Oleuropein3
Propyl gallate3
Plumbagin3
Pterostilbene3
Selenium3
Aflavin-3,3′-digallate3
VitK3,menadione3
Zerumbone2
Sorafenib (brand name Nexavar)2
Auranofin2
Phyllanthus emblica/Emblica officinalis/Amla / Indian Gooseberry2
Ascorbyl Palmitate2
Arctigenin2
Baicalin2
Biochanin A2
Brucea javanica2
Bacopa monnieri2
Butyrate2
Caffeic Acid Phenethyl Ester (CAPE)2
Hydroxycinnamic-acid2
Coenzyme Q102
Carica papaya leaf extract2
Cynara scolymus/Globe Artichoke/Artichoke Extract2
Dichloroacetophenone(2,2-)2
diet Short Term Fasting2
Eurycomanone2
Arsenic trioxide2
Ginkgolic acids2
γ-linolenic acid (Borage Oil)2
Graviola2
Grapeseed extract2
Naringin2
Niclosamide (Niclocide)2
Psoralidin2
EMF2
α-Santalol/Sandalwood oil2
Sulfasalazine2
Terpinen-4-ol / Tea Tree Oil2
Vitamin C (Ascorbic Acid)2
Vitamin D31
2-DeoxyGlucose1
3-bromopyruvate1
Glucose1
SonoDynamic Therapy UltraSound1
Zinc1
Ajoene (compound of Garlic)1
Fennel Oil/Foeniculum vulgare1
Aloe anthraquinones1
beta-glucans1
almonertinib1
bempedoic acid1
Bevacizumab (brand Avastin)1
temozolomide1
Bromelain1
borneol1
Bortezomib1
Bruteridin(bergamot juice)1
hydroxychloroquine1
Cat’s Claw1
Cynanbungeigenin C (CBC) and D (CBD)1
Cannabidiol1
Camptothecin1
irinotecan1
CUSP91
Dasatinib/Phyrago1
Dihydrocaffeic Acid1
diet FMD Fasting Mimicking Diet1
Echinacea1
Electrical Pulses1
Exercise1
Vitamin E1
ferumoxytol1
Vitamin A, Retinoic Acid1
Shilajit/Fulvic Acid1
Ginseng1
Germacranolide sesquiterpene lactone1
Siegesbeckia glabrescens1
HydroxyCitric Acid1
epipolythiodioxopiperazine / epipolythiopiperazine-2,5-dione1
Hibiscus sabdariffa1
Hops (Humulus lupulus)1
Hyperthermia1
Inoscavin A1
itraconazole1
Ivermectin1
Laetrile B17 Amygdalin1
Licorice1
doxorubicin1
Mushroom Chaga1
Oroxylin A1
Oleocanthal1
Proanthocyanidins1
sericin1
xanthohumol1
Gold NanoParticles1
Rauwolfia serpentina/Indian Snakeroot1
Oxaliplatin1
Selenium NanoParticles1
diet Plant based1
Salvia miltiorrhiza1
Spermidine1
tetrathiomolybdate1
Turmerones1
Vitexin1
Wogonin
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#:327 State#:% Dir#:1
wNotes=on sortOrder:rid,rpid
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