TumCG Cancer Research Results

TumCG, Tumor cell growth: Click to Expand ⟱
Source:
Type:
Normal cells grow and divide in a regulated manner through the cell cycle, which consists of phases (G1, S, G2, and M).
Cancer cells often bypass these regulatory mechanisms, leading to uncontrolled proliferation. This can result from mutations in genes that control the cell cycle, such as oncogenes (which promote cell division) and tumor suppressor genes (which inhibit cell division).
Scientific Papers found: Click to Expand⟱
2432- 2DG,    Inhibition of glycolytic enzyme hexokinase II (HK2) suppresses lung tumor growth
- in-vitro, Lung, H23 - in-vitro, Lung, KP2 - in-vivo, NA, NA
HK2↓, 2-DG, an inhibitor of HK2, inhibited human and mouse lung cancer cell growth through inducing cell apoptosis and autophagy.
Apoptosis↑,
TumAuto↑,
TumCG↓, these studies showed that the 2-DG, HK2 inhibitor, suppresses lung cancer cell growth in vivo.

5277- 3BP,    3-Bromopyruvate inhibits pancreatic tumor growth by stalling glycolysis, and dismantling mitochondria in a syngeneic mouse model
- in-vivo, PC, Panc02
HK2↓, It exerts potent anticancer effects by inhibiting hexokinase II enzyme (HK2) of the glycolytic pathway in cancer cells while not affecting the normal cells.
selectivity↑, it doesn’t affect the normal cells but strongly toxic to cancer cells
ATP↓, 3-BP killed 95% of Panc-2 cells at 15 μM concentration and severely inhibited ATP production by disrupting the interaction between HK2 and mitochondrial Voltage Dependent Anion Channel-1 (VDAC1) protein.
mtDam↑, Electron microscopy data revealed that 3-BP severely damaged mitochondrial membrane in cancer cells.
Dose↝, We further examined therapeutic effect of 3-BP in syngeneic mouse pancreatic cancer model by treating animals with 10, 15 and 20 mg/kg dose. 3-BP at 15 & 20 mg/kg dose level significantly reduced tumor growth by approximately 75-80% in C57BL/6 female
TumCG↓, 3-BP inhibit in vivo pancreatic tumor growth in C57BL/6 mouse model
Casp3↑, observed enhanced expression of active caspase-3 in tumor tissues exhibited apoptotic death.
Glycolysis↓, Notably, metabolomic data also revealed severe inhibition in glycolysis, NADP, ATP and lactic acid production in cancer cells treated with 40 μM 3-BP.
NADPH↓,
ATP↓,
ROS↑, 3-BP treatment produces increased levels of reactive oxygen species (ROS), which causes DNA damage with reduction of free glutathione levels [11].
DNAdam↑,
GSH↓,
Bcl-2↓, Further, treatment with 40 µM of 3-BP suppressed BCL2L1 expression and causing activation of mitochondrial caspases
Casp↑,
lactateProd↓, Metabolic inhibition of glucose consumption and lactic acid production in cancer cells treated with 3-BP

5274- 3BP,    ME3BP-7 is a targeted cytotoxic agent that rapidly kills pancreatic cancer cells expressing high levels of monocarboxylate transporter MCT1
- in-vitro, PC, NA
eff↑, novel microencapsulated formulation of 3BP (ME3BP-7), which is effective against a variety of PDAC cells in vitro and remains stable in serum.
TumCG↓, Furthermore, systemically administered ME3BP-7 significantly reduces pancreatic cancer growth and metastatic spread in multiple orthotopic models of pancreatic cancer with manageable toxicity.
TumMeta↓,
toxicity↝,
Glycolysis↓, The anticancer effects of 3BP were initially attributed to inhibition of glycolysis (Ganapathy-Kanniappan et al., 2009;
toxicity↓, Our previous work demonstrated that microencapsulation of 3BP reduces its toxicity (Chapiro et al., 2014).
Dose↝, we were only able to reliably deliver multiple doses of the drug intravenously (i.v.), and the number of injections and time periods over which we could administer the drug were limited.

5258- 3BP,    3-bromopyruvate: Targets and outcomes
- Review, Var, NA
Glycolysis↓, The pyruvate mimetic 3-bromopyruvate (3-BP) is generally presented as an inhibitor of glycolysis and has shown remarkable efficacy in not only preventing tumor growth, but even eradicating existant tumors in animal studies.
TumCG↓,

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

5472- AF,    Auranofin induces apoptosis and necrosis in HeLa cells via oxidative stress and glutathione depletion
- in-vitro, Cerv, HeLa
TrxR↓, Auranofin (Au), an inhibitor of thioredoxin reductase, is a known anti‑cancer drug
AntiCan↑,
TumCG↓, Au inhibited the growth of HeLa cells with an IC50 of ~2 µM at 24 h.
Apoptosis↑, This agent induced apoptosis and necrosis, accompanied by the cleavage of poly (ADP‑ribose) polymerase and loss of mitochondrial membrane potential.
necrosis↑,
cl‑PARP↑,
MMP↓,
ROS↑, With respect to the levels of ROS and GSH, Au increased intracellular O2•- in the HeLa cells and induced GSH depletion.
GSH↓,
eff↓, The antioxidant, N‑acetyl cysteine, not only attenuated apoptosis and necrosis in the Au‑treated HeLa cells, but also decreased the levels of O2•- and GSH depletion in the cells.

5468- AF,    The gold complex auranofin: new perspectives for cancer therapy
- Review, Var, NA
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

1000- AG,  5-FU,    Characterization and anti-tumor bioactivity of astragalus polysaccharides by immunomodulation
- vitro+vivo, BC, 4T1
TumCG↓,
TumCCA↑, cell cycle arrest (G2 phase)
Apoptosis↑,
*IL2↑, in peripheral blood
*TNF-α↑, in peripheral blood
*IFN-γ↑, in peripheral blood

944- AG,    Astragalus saponins inhibit cell growth, aerobic glycolysis and attenuate the inflammatory response in a DSS-induced colitis model
- vitro+vivo, CRC, NA
Glycolysis↓,
lactateProd↓,
TumCG↓,

5444- AG,    A Systematic Review of Phytochemistry, Pharmacology and Pharmacokinetics on Astragali Radix: Implications for Astragali Radix as a Personalized Medicine
- Review, Var, NA
*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

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.

5434- AG,    Recent Advances in the Mechanisms and Applications of Astragalus Polysaccharides in Liver Cancer Treatment: An Overview
- Review, Liver, NA
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↓, 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

5437- AG,    Modulation of PD-L1 by Astragalus polysaccharide attenuates the induction of melanoma stem cell properties and overcomes immune evasion
- in-vivo, Melanoma, B16-F10
CSCs↓, APS attenuated the tumor sphere formation of MSCs in vitro as well as the tumorigenicity in vivo.
CD133↓, It also decreased the expression of CD133, BMI1 and CD47.
BMI1↓,
PD-L1↓, it was confirmed that APS inhibited the induction of MSCs by down-regulating PD-L1 expression.
TumCG↓, Accordingly, the CSC properties were also attenuated, accompanied by a slower tumor growth rate. F

5436- AG,    Therapeutic Effect of Astragalus Polysaccharides on Hepatocellular Carcinoma H22-Bearing Mice
- in-vivo, HCC, NA
TumCG↓, APS inhibited the growth of H22 cells with a tumor inhibition rate in the APS 400 mg·kg−1 group of 59.01%
BAX↑, APS increased Bax protein expression and decreased Bcl-2 protein expression; these proteins are apoptosis-regulating factors responsible for cell death or survival.
Bcl-2↓,
IL2↑, These results indicated that APS promotes the expression of IL-2, IL-6, and TNF-α as an H22 tumor treatment mechanism
IL6↑,
TNF-α↑,
toxicity↓, APS could inhibit H22 tumor with low toxicity.

4400- AgNPs,  Rad,    Differential cytotoxic and radiosensitizing effects of silver nanoparticles on triple-negative breast cancer and non-triple-negative breast cells
- in-vitro, BC, MCF-7 - in-vitro, Nor, MCF10 - in-vitro, BC, MDA-MB-231 - in-vitro, BC, BT549 - in-vivo, BC, MDA-MB-231
ROS↑, AgNPs is known to cause dose-dependent toxicities, including induction of oxidative stress and DNA damage, which can lead to cell death.
DNAdam↑,
selectivity↑, We show that AgNPs are highly cytotoxic toward TNBC cells at doses that have little effect on nontumorigenic breast cells or cells derived from liver, kidney, and monocyte lineages.
TumCG↓, reduce TNBC growth and improve radiation therapy.
RadioS↑,
Dose↝, s 23±14 nm: particles were diluted to 40 μg/mL. 25 μg/mL AgNP dilution for 24 hours. zeta potential of AgNPs in water at pH 7 was approximately −36 mV, indicating good colloidal stability.
selectivity↑, Depending on AgNP dose, all three TNBC cell lines were 5- to 10-fold more sensitive to AgNP exposure than the nontumorigenic breast cells.
other↝, this study demonstrate that the cytotoxicity was dependent on exposure of cells to intact AgNPs and not due to Ag+ ions
eff↓, toxicity of AgNPs was significantly reduced in MDA-MB-231, MCF-7, and MCF-10A cells following pretreatment with GSH
eff↑, Selective depletion of GSH by BSO resulted in increased AgNP toxicity in all cell lines.
γH2AX↑, AgNPs significantly increased γH2AX in these cells compared to radiation alone.
Dose↓, Strikingly, an AgNP dose of as little as 1 μg/mL resulted in a dose enhancement of IR treatment (approximately 2-fold at the 2 Gy dose) f
eff↑, Moreover, intratumoral injection of AgNPs with or without radiation treatment can inhibit the growth of TNBC xenografts in mice

4413- AgNPs,  Anzaroot,    Green synthesis of silver nanoparticles from plant Astragalus fasciculifolius Bioss and evaluating cytotoxic effects on MCF7 human breast cancer cells
- in-vitro, BC, MCF-7
chemoP↑, These compounds have been shown to effectively treat heart diseases and inhibit cancer cell growth while also alleviating chemotherapy side effects.
TumCG↓,
eff↑, anzroot plant can be effectively used as a reducing agent for AgNPs synthesis, and AgNPs have the potential to be used effectively in cancer therapy methods and to inhibit the growth of cancer cells.
CellMemb↑, As the AgNPs concentration increased, the permeability of the membrane increased
selectivity↑, Cancer cells exhibit higher permeability and retention, allowing for preferential interaction with SNPs due to their nanoscale size
ROS↑, AgNPs respond to intracellular signaling through ROS activation, and p53-mediated apoptosis is notably effective when using AgNPs
P53↑,

4407- AgNPs,    Green Synthesis and Characterization of Silver Nanoparticles from Eclipta alba and Its Activity Against Triple-Negative Breast Cancer Cell Line (MDA-MB-231)
- in-vitro, BC, MDA-MB-231
antiOx↑, Further in vitro anti-oxidant analysis results revealed that green synthesized AgNPs showed 2.6-fold higher anti-oxidant potential (IC50 15.70 g/ml) than that of aqueous plant leaf extract (IC50 39.80 g/ml).
TumCG↓, Eclipta alba leaf extract actively bonded with silver nanoparticles suppresses the MDA-MB-231 cells growth through high antioxidant characters and anti-leishmanial activity.

4362- AgNPs,    Enhancing Colorectal Cancer Radiation Therapy Efficacy using Silver Nanoprisms Decorated with Graphene as Radiosensitizers
- in-vitro, CRC, HCT116 - in-vitro, CRC, HT29 - in-vivo, NA, NA
eff↑, large surface area-to-volume ratio, which can be exploited in cancer radiotherapy to locally enhance the radiation dose deposition in tumors
TumCG↓, Treatment with nanoparticles and a single radiation dose of 10 Gy significantly reduces the growth of colorectal tumors
OS↑, increases the survival time as compared to treatment with radiation only
RadioS↑, combine standard-dose radiotherapy with radiosensitizers to enhance the radiation therapy efficacy locally within tumors while sparing adjacent healthy tissues
eff↑, suggested that graphene enhances the cellular uptake when combined with metals in nanocomposites
ROS↑, ROS, the most potent of these free radicals, can travel to and indirectly damage DNA
DNAdam↑,
eff↝, PEGylated GQD-decorated Silver Nanoprisms (pGAgNPs) show better intracellular uptake as compared to PEGylated Silver Nanoprisms (pAgNPs)

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↓,

4363- AgNPs,    Immunomodulatory properties of silver nanoparticles contribute to anticancer strategy for murine fibrosarcoma
- in-vivo, fibroS, NA
TumVol↓, incidence and size of fibrosarcoma were reduced or delayed when murine fibrosarcoma groups were treated by AgNP-MSA
TNF-α↓, TNF-α, IL-6 and IL-1β these cytokines were found to be downregulated after treatment with AgNP-MSA
IL6↓,
IL1β↓,
*toxicity↝, liver sections were found to have normal architecture in all treated groups except those treated at the 9 and 10 mg/kg b.w. doses
TumCG↓, treatment with AgNPs, the logistic growth of the tumor incidence was significantly lower (
selectivity↑, MSA-AgNPs aggregated instantly in response to the acidic extracellular pH of solid tumors, leading to greatly enhanced uptake by cancer cells
selectivity↑, Because the particle size in the study was approximately 10 nm, any AgNP that escaped entry into the tumor microenvironment and entered the systemic circulation was effectively cleared from the body.
Weight↑, AgNP-MSA not only inhibited the tumor incidence but also helped to overcome the progressive body weight loss of tumor-bearing mice.
ROS↑, anticancer property demonstrated by AgNP can be attributed to this increase in oxidative stress in the tumor microenvironment.
NO↑, AgNPs significantly increased the oxygen free radical and NO levels in the tumor microenvironment, which oppose hypoxia.

4551- AgNPs,  Fenb,    Ångstrom-Scale Silver Particles as a Promising Agent for Low-Toxicity Broad-Spectrum Potent Anticancer Therapy
- in-vivo, Lung, NA
eff↑, Here, a pure physical method is used to efficiently fabricate very small silver particles even approaching the Ångstrom (Ång) dimension.
eff↑, Fructose is used as a dispersant and stabilizer to coat the Ång-scale silver particles (AgÅPs).
Apoptosis↑, (F-AgÅPs) can enter and accumulate in multiple cultured cancer cell lines to induce apoptotic death, whereas most normal cells are resistant to the efficacious dose of F-AgÅPs;
selectivity↓,
TumCG↓, intravenous administration of F-AgÅPs potently inhibits the growth of pancreatic and lung cancer xenografts in nude mice, without inducing notable toxic effects on the healthy tissues.

4593- AgNPs,  Chit,    Chitosan-coated silver nanoparticles promoted antibacterial, antibiofilm, wound-healing of murine macrophages and antiproliferation of human breast cancer MCF 7 cells
- in-vitro, BC, MCF-7
*Bacteria↓, Ch-AgNPs (8–48 nm) exhibited significant antibacterial and antibiofilm activity.
*Wound Healing↑, Ch-AgNPs promoted wound healing activity at 75 and 100 μg mL−1 after 24 h.
TumCG↓, Ch-AgNPs effective inhibited the MCF-7 human breast cancer cells at 100 μg mL−1 after 24 h.

374- AgNPs,    Silver nanoparticles selectively treat triple‐negative breast cancer cells without affecting non‐malignant breast epithelial cells in vitro and in vivo
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231 - in-vivo, NA, NA
ER Stress↑,
DNAdam↑,
ROS↑,
Apoptosis↑,
GSH/GSSG↓, MDA‐MB‐231
NADPH/NADP+↓, MDA‐MB‐231
TumCG↓,
UPR↑, initiating UPR

367- AgNPs,    Presence of an Immune System Increases Anti-Tumor Effect of Ag Nanoparticle Treated Mice
- in-vivo, NA, NA
ROS↑,
mtDam↑,
TumCG↓,

358- AgNPs,    Preparation of triangular silver nanoparticles and their biological effects in the treatment of ovarian cancer
- vitro+vivo, Ovarian, SKOV3
TumCCA↑, arrested the cell cycle in G0/G1 phase
ROS↑,
Casp3↑,
TumCG↓,
cycD1/CCND1↓, and cyclinA2

379- AgNPs,    Effects of green-synthesized silver nanoparticles on lung cancer cells in vitro and grown as xenograft tumors in vivo
- in-vivo, Lung, H1299
NF-kB↓,
Bcl-2↓,
Casp3↑,
survivin↑,
TumCG↓, suppressed tumor growth

380- AgNPs,  QC,  CA,  Chit,    Quercetin- and caffeic acid-functionalized chitosan-capped colloidal silver nanoparticles: one-pot synthesis, characterization, and anticancer and antibacterial activities
- in-vitro, MG, U118MG
TumCG↓, cell viability has constantly decreased by increasing the concentration

2647- AL,    The Mechanism in Gastric Cancer Chemoprevention by Allicin
- Review, GC, NA
ChemoSen↓, Experiments have shown that allicin can be chemopreventive to gastric cancer
TumCG↓, by inhibiting the growth of cancer cells, arresting cell cycle at G2/M phase, endoplasmic reticulum (ER) stress, and mitochondria-mediated apoptosis, which includes the caspase-dependent/-independent pathways and death receptor pathway.
TumCCA↑,
ER Stress↑,
Apoptosis↑,
Casp↑,
DR5↑, DR5 (death receptor 5) was found to be upregulated following allicin treatment

2648- AL,    Allicin Inhibits Osteosarcoma Growth by Promoting Oxidative Stress and Autophagy via the Inactivation of the lncRNA MALAT1-miR-376a-Wnt/β-Catenin Signaling Pathway
- in-vitro, OS, SaOS2 - in-vivo, OS, NA
ROS↑, Allicin inhibited osteosarcoma growth and promoted oxidative stress and autophagy via MALATI-miR-376a
TumCG↓,
TumAuto↑,
Wnt↓, allicin promotes oxidative stress and autophagy to inhibit osteosarcoma growth by inhibiting the Wnt/β-catenin pathway in vivo and in vitro.
β-catenin/ZEB1↓,
MALAT1↓, Allicin Inhibited OS Growth by Promoting Oxidative Stress and Autophagy via Inactivation of the MALAT1-miR-376a-Wnt/β-Catenin Signal Pathway Axis In Vitro and In Vivo

1290- AL,    Effect of allicin on the expression of Bcl-2 and Bax protein in LM-8 cells
- in-vitro, OS, LM8
Bcl-2↓,
BAX↑,
Apoptosis↑,
TumCG↓,

544- AL,    Garlic constituents for cancer prevention and therapy: From phytochemistry to novel formulations
Risk↓,
ChemoSideEff↓,
TumCG↓,
NF-kB⇅, alter

5168- AL,    Allicin (from garlic) induces caspase-mediated apoptosis in cancer cells
- in-vitro, Var, NA
TumCG↓, We found that allicin inhibited the growth of cancer cells of murine and human origin.
Casp3↑, Furthermore, activation of caspases-3, -8 and -9 and cleavage of poly(ADP-ribose) polymerase were induced by allicin
Casp8↑,
Casp9↑,
chemoPv↑, antiproliferative effects of allicin and partly account for the chemopreventive action of garlic extracts reported by earlier workers.

288- ALA,  HCA,  CAP,  Octr,    Tumor regression with a combination of drugs interfering with the tumor metabolism: efficacy of hydroxycitrate, lipoic acid and capsaicin
TumCG↓, delays tumor growth in mice

285- ALA,  HCA,    Tolerance of oral lipoid acid and hydroxycitrate combination in cancer patients: first approach of the cancer metabolism research group
- Human, Var, NA
PI3K↝,
AMPK↝,
TumCG↓,
*toxicity↓, No hepatic toxicity found, no weight loss, no hypoglycemia
Weight∅,

280- ALA,    Alpha‐lipoic acid inhibits lung cancer growth via mTOR‐mediated autophagy inhibition
- in-vivo, Lung, A549
p‑mTOR↑, significantly increased mTOR phosphorylation level by 76.9%
TumCG↓, LA suppressed lung cancer growth in mice.
TumAuto↓, (note this research paper takes the approach of wanting to reduce autophagy)
p‑P70S6K↑, phosphorylation level of p70S6K, a downstream target of mTOR, was increased by 83.2% when compared with controls

290- ALA,  HCA,    A combination of alpha lipoic acid and calcium hydroxycitrate is efficient against mouse cancer models: preliminary results
- vitro+vivo, Melanoma, B16-F10
TumCG↓,
OS↑,

291- ALA,  HCA,  MET,  Dicl,    Metabolic therapies inhibit tumor growth in vivo and in silico
- in-vivo, Melanoma, B16-F10 - in-vivo, Lung, LL/2 (LLC1) - in-vivo, Bladder, MBT-2
TumCG↓,

296- ALA,    Lipoic acid inhibits cell proliferation of tumor cells in vitro and in vivo
- vitro+vivo, neuroblastoma, SK-N-SH - vitro+vivo, BC, SkBr3
TumCG↓,
Casp3↑,

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↑,

258- ALA,    Effects of α-lipoic acid on cell proliferation and apoptosis in MDA-MB-231 human breast cells
- in-vitro, BC, MDA-MB-231
TumCG↓, inhibited growth
p‑Akt↓,
Akt↓,
HER2/EBBR2↓, ErbB2 and ErbB3 protein and mRNA expressions
Bcl-2↓,
BAX↑,
Casp3↑,

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

5326- ALC,    L-Carnitine Is an Endogenous HDAC Inhibitor Selectively Inhibiting Cancer Cell Growth In Vivo and In Vitro
- vitro+vivo, Liver, HepG2
TumCG↓, Here we found that (1) LC treatment selectively inhibited cancer cell growth in vivo and in vitro;
P21↑, (2) LC treatment selectively induces the expression of p21cip1 gene, mRNA and protein in cancer cells
ac‑H3↑, (4) LC increases histone acetylation and induces accumulation of acetylated histones both in normal thymocytes and cancer cells
HDAC↓, (5) LC directly inhibits HDAC I/II activities via binding to the active sites of HDAC and induces histone acetylation and lysine-acetylation accumulation in vitro;
*ATP↑, LC is able to generate ATP in normal mouse thymocytes, but not in hepatic HepG2 and SMMC-7721 cancer cells.
selectivity↑,
ac‑H4↑, LC dose-dependently increased acetylation of H3 and H4 (

1349- And,    Andrographolide promoted ferroptosis to repress the development of non-small cell lung cancer through activation of the mitochondrial dysfunction
- in-vitro, Lung, H460 - in-vitro, Lung, H1650
TumCG↓,
TumMeta↓,
Ferroptosis↑,
ROS↑,
MDA↑,
Iron↑,
GSH↓, lipid ROS reduced glutathione (GSH) accumulation
GPx4↓,
xCT↓, SLC7A11
MMP↓,
ATP↓,

1348- And,    Andrographolide Inhibits ER-Positive Breast Cancer Growth and Enhances Fulvestrant Efficacy via ROS-FOXM1-ER-α Axis
- in-vitro, BC, MCF-7 - in-vitro, BC, T47D - in-vivo, NA, NA
ERα/ESR1↓,
TumCG↓,
ROS↑,
FOXM1↓,
eff↑, In addition, AD in combination with fulvestrant (FUL) synergistically down-regulated ER-α expression to inhibit ER-positive breast cancer both in vitro and in vivo.

4759- antiOx,  Chemo,    Potential Contributions of Antioxidants to Cancer Therapy: Immunomodulation and Radiosensitization
- Review, Var, NA
TumCD↑, curcumin has been shown to modulate immunoediting processes including resurrecting immune surveillance mechanisms to help eradicate cancer cells
TumCG↓, studies by Lee-Chang et al34 have shown that administration of resveratrol, a dietary polyphenol compound possessing antioxidant properties at low doses that are nontoxic to immune cells, inhibits lung metastasis of breast cancer tumor.
ROS⇅, Of importance, resveratrol can exert both antioxidant and pro-oxidant properties depending on its concentration and cell types used
eff↑, Wang et al36 have demonstrated that a combination of fish oil and selenium that possesses anti-inflammatory and antioxidant activities exerted synergistic effects in suppressing lung tumor growth mediated via decreasing the population of splenic Treg
RadioS↑, Several nutritional cancer chemopreventive compounds having antioxidant properties have been documented to potentiate radiation therapy–induced cytotoxic effects on cancer cells while reducing its toxicity on normal surrounding tissues.77-86
TumCG↓, soy isoflavone component genistein on prostate cancer demonstrated that both soy and genistein inhibited the growth of in vitro human PC-3 prostate cancer cells and in vivo orthotopic PC-3 tumors
OS↑, While a statistically significant improved survival rate either at 1 year or 5 years was associated with melatonin supplementation
toxicity∅, 9 RCTs reported no differences in the toxicities by antioxidants supplementation
toxicity↑, and 1 RCT with vitamin A reported increased toxicity.

1151- Api,    Plant flavone apigenin inhibits HDAC and remodels chromatin to induce growth arrest and apoptosis in human prostate cancer cells: In vitro and in vivo study
- in-vitro, Pca, PC3 - in-vitro, Pca, 22Rv1 - in-vivo, NA, NA
TumCCA↑,
Apoptosis↑,
HDAC↓, HDAC1 and HDAC3
P21↑,
BAX↑,
TumCG↓,
Bcl-2↓,
Bax:Bcl2↑, shifting the bax/bcl2 ratio in favor of apoptosis
HDAC1↓,
HDAC3↓,

1564- Api,    Apigenin-induced prostate cancer cell death is initiated by reactive oxygen species and p53 activation
- in-vitro, Pca, 22Rv1 - in-vivo, NA, NA
MDM2↓, downregulation of MDM2 protein
NF-kB↓, Exposure of 22Rv1 cells to 20 μM apigenin caused a decrease in NF-κB/p65 transcriptional activity by 24% at 12 h, which was further decreased to 41% at 24 h
p65↓,
P21↑,
ROS↑, Apigenin at these doses resulted in ROS generation
GSH↓, which was accompanied by rapid glutathione depletion
MMP↓, disruption of mitochondrial membrane potential
Cyt‑c↑, cytosolic release of cytochrome c
Apoptosis↑,
P53↑, accumulation of a p53 fraction to the mitochondria, which was rapid and occurred between 1 and 3 h after apigenin treatment
eff↓, All these effects were significantly blocked by pretreatment of cells with the antioxidant N-acetylcysteine
Bcl-xL↓,
Bcl-2↓,
BAX↑,
Casp↑, triggering caspase activation
TumCG↓, in vivo mice
TumVol↓, tumor volume was inhibited by 44 and 59%
TumW↓, wet weight of tumor was decreased by 41 and 53%

2634- Api,    Apigenin induces both intrinsic and extrinsic pathways of apoptosis in human colon carcinoma HCT-116 cells
- in-vitro, CRC, HCT116
TumCG↓, Apigenin exerted cytotoxic effect on the cells via inhibiting cell growth in a dose-time-dependent manner and causing morphological changes, arrested cell cycle progression at G0/G1 phase
TumCCA↑,
MMP↓, decreased mitochondrial membrane potential of the treated cells
ROS↑, Apigenin increased respective ROS generation and Ca2+ release and thereby, caused ER stress in the treated cells.
Ca+2↑,
ER Stress↑,
mtDam↑, together with damaged mitochondrial membrane, and upregulated protein expression of CHOP, DR5, cleaved BID, Bax, cytochrome c, cleaved caspase-3, cleaved caspase-8 and cleaved caspase-9, which triggered apoptosis of the cells.
CHOP↑,
DR5↑,
cl‑BID↑,
BAX↑,
Cyt‑c↑,
cl‑Casp3↑,
cl‑Casp8↑,
cl‑Casp9↑,
Apoptosis↑,

2585- Api,    Apigenin inhibits the proliferation of adenoid cystic carcinoma via suppression of glucose transporter-1
- in-vitro, ACC, NA
GLUT1↓, expression levels of GLUT‑1 were significantly decreased following treatment in a dose- and time-dependent manner.
TumCG↓, inhibition of ACC-2 cell growth by apigenin may be due to the decreased expression of GLUT-1


Showing Research Papers: 1 to 50 of 574
Page 1 of 12 Next

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 574

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   Ferroptosis↑, 2,   GPx4↓, 3,   GSH↓, 5,   GSH/GSSG↓, 1,   Iron↑, 1,   c-Iron↑, 1,   lipid-P↑, 1,   MDA↑, 1,   NADPH/NADP+↓, 1,   ROS↑, 17,   ROS⇅, 1,   TrxR↓, 2,   xCT↓, 2,  

Mitochondria & Bioenergetics ⓘ

AIF↑, 1,   ATP↓, 5,   MMP↓, 7,   mtDam↑, 3,  

Core Metabolism/Glycolysis ⓘ

ACSL4↑, 1,   AMPK↑, 4,   AMPK↝, 1,   FDG↓, 1,   GAPDH↓, 1,   Glycolysis↓, 5,   HK2↓, 2,   lactateProd↓, 2,   NADPH↓, 1,   PDH↑, 1,   SIRT1↓, 1,   SREBP1↓, 1,  

Cell Death ⓘ

Akt↓, 7,   p‑Akt↓, 1,   Apoptosis↑, 14,   BAX↑, 8,   Bax:Bcl2↑, 1,   Bcl-2↓, 9,   Bcl-xL↓, 1,   cl‑BID↑, 1,   Casp↑, 4,   Casp3↑, 8,   cl‑Casp3↑, 1,   Casp8↑, 1,   cl‑Casp8↑, 1,   Casp9↑, 2,   cl‑Casp9↑, 1,   Cyt‑c↑, 3,   DR5↑, 2,   Fas↓, 1,   Fas↑, 1,   FasL↓, 1,   Ferroptosis↑, 2,   JNK↓, 2,   MDM2↓, 1,   necrosis↑, 1,   survivin↑, 1,   TumCD↑, 1,  

Kinase & Signal Transduction ⓘ

HER2/EBBR2↓, 1,  

Transcription & Epigenetics ⓘ

ac‑H3↑, 1,   ac‑H4↑, 1,   other↓, 1,   other↝, 1,  

Protein Folding & ER Stress ⓘ

CHOP↑, 1,   ER Stress↑, 3,   UPR↑, 1,  

Autophagy & Lysosomes ⓘ

Beclin-1↑, 1,   TumAuto↓, 1,   TumAuto↑, 3,  

DNA Damage & Repair ⓘ

DNAdam↑, 6,   P53↑, 3,   cl‑PARP↑, 1,   γH2AX↑, 1,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 2,   P21↑, 4,   TumCCA↑, 7,  

Proliferation, Differentiation & Cell State ⓘ

BMI1↓, 1,   CD133↓, 2,   CD44↓, 1,   CSCs↓, 3,   EMT↓, 5,   FOXM1↓, 1,   GSK‐3β↓, 2,   HDAC↓, 2,   HDAC1↓, 1,   HDAC3↓, 1,   mTOR↓, 5,   p‑mTOR↑, 1,   NOTCH1↓, 3,   NOTCH3↓, 1,   p‑P70S6K↑, 1,   PI3K↓, 5,   PI3K↝, 1,   TumCG↓, 52,   Wnt↓, 3,  

Migration ⓘ

Ca+2↑, 1,   E-cadherin↑, 2,   MALAT1↓, 1,   miR-133a-3p↑, 1,   MMP2↓, 1,   MMP9↓, 3,   N-cadherin↓, 1,   p‑SMAD2↓, 1,   Snail↓, 1,   TGF-β↓, 1,   TGF-β1↓, 1,   TumCI↓, 6,   TumCMig↓, 4,   TumCP↓, 7,   TumMeta↓, 4,   Twist↓, 1,   Vim↓, 3,   β-catenin/ZEB1↓, 4,  

Angiogenesis & Vasculature ⓘ

angioG↑, 1,   EGFR↓, 2,   EGR4↓, 1,   Hif1a↓, 1,   NO↑, 1,   VEGF↓, 3,  

Barriers & Transport ⓘ

CellMemb↑, 1,   GLUT1↓, 1,   P-gp↓, 2,  

Immune & Inflammatory Signaling ⓘ

CXCR4↓, 1,   IL12↑, 1,   IL1β↓, 1,   IL2↑, 2,   IL6↓, 2,   IL6↑, 1,   Imm↑, 2,   Inflam↓, 1,   NF-kB↓, 5,   NF-kB⇅, 1,   p65↓, 1,   PD-L1↓, 2,   TNF-α↓, 2,   TNF-α↑, 2,  

Hormonal & Nuclear Receptors ⓘ

ERα/ESR1↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   BioAv↝, 2,   ChemoSen↓, 1,   ChemoSen↑, 4,   Dose↓, 1,   Dose↝, 5,   eff↓, 4,   eff↑, 19,   eff↝, 2,   Half-Life↓, 1,   MDR1↓, 1,   RadioS↑, 3,   selectivity↓, 1,   selectivity↑, 7,  

Clinical Biomarkers ⓘ

EGFR↓, 2,   ERα/ESR1↓, 1,   FOXM1↓, 1,   HER2/EBBR2↓, 1,   IL6↓, 2,   IL6↑, 1,   PD-L1↓, 2,  

Functional Outcomes ⓘ

AntiCan↑, 2,   AntiTum↑, 2,   chemoP↑, 3,   chemoPv↑, 1,   ChemoSideEff↓, 1,   OS↑, 3,   QoL↑, 2,   Risk↓, 1,   toxicity↓, 5,   toxicity↑, 2,   toxicity↝, 1,   toxicity∅, 1,   TumVol↓, 2,   TumW↓, 1,   Weight↑, 1,   Weight∅, 1,  
Total Targets: 172

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 2,   GSH↑, 1,   lipid-P↓, 1,   ROS↓, 1,  

Metal & Cofactor Biology ⓘ

IronCh↑, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↑, 1,  

Core Metabolism/Glycolysis ⓘ

GlucoseCon↑, 1,  

Transcription & Epigenetics ⓘ

Ach↑, 1,   other↓, 1,   other↝, 1,  

Immune & Inflammatory Signaling ⓘ

IFN-γ↑, 1,   IL1β↓, 1,   IL2↑, 1,   IL6↓, 1,   Imm↑, 1,   Inflam↓, 1,   TNF-α↑, 1,  

Synaptic & Neurotransmission ⓘ

ChAT↑, 1,  

Drug Metabolism & Resistance ⓘ

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

Clinical Biomarkers ⓘ

IL6↓, 1,  

Functional Outcomes ⓘ

memory↑, 1,   neuroP↑, 1,   toxicity↓, 1,   toxicity↝, 1,   Wound Healing↑, 1,  

Infection & Microbiome ⓘ

Bacteria↓, 1,  
Total Targets: 28

Scientific Paper Hit Count for: TumCG, Tumor cell growth
26 Curcumin
23 Magnetic Fields
17 Phenethyl isothiocyanate
15 Quercetin
14 Berberine
13 Silver-NanoParticles
13 Shikonin
12 Chemotherapy
12 Sulforaphane (mainly Broccoli)
11 EGCG (Epigallocatechin Gallate)
11 Magnetic Field Rotating
10 Capsaicin
10 Baicalein
10 Vitamin C (Ascorbic Acid)
9 Alpha-Lipoic-Acid
9 Silymarin (Milk Thistle) silibinin
9 Garcinol
8 Astragalus
8 Apigenin (mainly Parsley)
8 Artemisinin
8 Resveratrol
8 salinomycin
8 diet FMD Fasting Mimicking Diet
8 Bicarbonate(Sodium)
8 Phenylbutyrate
8 Pterostilbene
8 Urolithin
7 HydroxyCitric Acid
7 Ashwagandha(Withaferin A)
7 Boron
7 Boswellia (frankincense)
7 Dichloroacetate
7 Gambogic Acid
6 Radiotherapy/Radiation
6 Allicin (mainly Garlic)
6 Betulinic acid
6 immunotherapy
6 Deguelin
6 diet Methionine-Restricted Diet
6 Sulfasalazine
6 Magnolol
6 Lycopene
6 Magnesium
6 Rosmarinic acid
5 chitosan
5 Metformin
5 Berbamine
5 Cisplatin
5 Chrysin
5 Coenzyme Q10
5 Gemcitabine (Gemzar)
5 Fisetin
5 Honokiol
5 Juglone
4 3-bromopyruvate
4 Melatonin
4 Atorvastatin
4 Brucea javanica
4 Caffeic Acid Phenethyl Ester (CAPE)
4 Emodin
4 Luteolin
4 Piperine
4 Piperlongumine
4 Selenite (Sodium)
4 Thymoquinone
4 Vitamin K2
4 VitK3,menadione
3 Astaxanthin
3 Baicalin
3 Bufalin/Huachansu
3 brusatol
3 Bruteridin(bergamot juice)
3 Butyrate
3 Carvacrol
3 Celastrol
3 Chlorogenic acid
3 Selenium NanoParticles
3 Citric Acid
3 Photodynamic Therapy
3 Genistein (soy isoflavone)
3 Graviola
3 Hydrogen Gas
3 Niclosamide (Niclocide)
3 Propyl gallate
3 Plumbagin
3 Aflavin-3,3′-digallate
2 2-DeoxyGlucose
2 Auranofin
2 Fenbendazole
2 Caffeic acid
2 Andrographis
2 doxorubicin
2 Ascorbyl Palmitate
2 Paclitaxel
2 Dipyridamole
2 Biochanin A
2 Bifidobacterium
2 Bromelain
2 Oxygen, Hyperbaric
2 diet Short Term Fasting
2 Disulfiram
2 Copper and Cu NanoParticles
2 Ellagic acid
2 Gallic acid
2 tamoxifen
2 Hydroxycinnamic-acid
2 HydroxyTyrosol
2 Methylene blue
2 Oroxylin-A
2 Oleuropein
2 Orlistat
2 Psoralidin
2 Hyperthermia
2 Oxaliplatin
2 Ursolic acid
1 5-fluorouracil
1 Anzaroot, Astragalus fasciculifolius Bioss
1 octreotide
1 Diclofenac
1 Acetyl-l-carnitine
1 Anti-oxidants
1 5-Aminolevulinic acid
1 Aloe anthraquinones
1 beta-glucans
1 temozolomide
1 Bacopa monnieri
1 Caffeine
1 Carnosic acid
1 urea
1 Cat’s Claw
1 Cannabidiol
1 Celecoxib
1 Chocolate
1 Cinnamon
1 Calorie Restriction Mimetics
1 Bicalutamide
1 Dichloroacetophenone(2,2-)
1 Bortezomib
1 Docosahexaenoic Acid
1 diet Ketogenic
1 diet Plant based
1 Zinc
1 Evodiamine
1 PXD, phenoxodiol
1 Sorafenib (brand name Nexavar)
1 Electrical Pulses
1 erastin
1 Fucoidan
1 Shilajit/Fulvic Acid
1 Galloflavin
1 Ginger/6-Shogaol/Gingerol
1 Glabrescione B
1 Grapeseed extract
1 Inositol
1 itraconazole
1 Ivermectin
1 Laetrile B17 Amygdalin
1 mebendazole
1 metronomic chemo
1 Methylglyoxal
1 Mushroom Chaga
1 Naringin
1 Nimbolide
1 Noscapine
1 Parthenolide
1 raloxifen
1 Salvia officinalis
1 Vorinostat
1 Selenium
1 irinotecan
1 Salvia miltiorrhiza
1 Spermidine
1 Saikosaponin B1 and D
1 Sutherlandioside D
1 Taurine
1 Tomatine
1 Tumor Treating Fields
1 Vitamin B1/Thiamine
1 Vitamin B5,Pantothenic Acid
1 Transarterial Chemoembolization
1 Whole Body Vibration
1 γ-Tocotrienol
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#:323  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

 

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