cMET Cancer Research Results

cMET, cellular hepatocyte growth factor receptor: Click to Expand ⟱
Source:
Type:
c-MET, also known as the hepatocyte growth factor receptor (HGFR), is a receptor tyrosine kinase that plays a crucial role in various cellular processes, including cell proliferation, survival, migration, and differentiation. It is activated by its ligand, hepatocyte growth factor (HGF). Dysregulation of the c-MET signaling pathway has been implicated in several types of cancer.

c-Met is often overexpressed or mutated in cancer and is associated with poor prognosis, increased metastasis, and resistance to therapies.
Scientific Papers found: Click to Expand⟱
308- Api,    Apigenin Inhibits Cancer Stem Cell-Like Phenotypes in Human Glioblastoma Cells via Suppression of c-Met Signaling
- in-vitro, GBM, U87MG - in-vitro, GBM, U373MG
cMET↓,
Akt↓,
Nanog↓,
SOX2↓, Sox2

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

3156- Ash,    Withaferin A: From ayurvedic folk medicine to preclinical anti-cancer drug
- Review, Var, NA
MAPK↑, Figure 3
p38↑,
BAX↑,
BIM↑,
CHOP↑,
ROS↑,
DR5↑,
Apoptosis↑,
Ferroptosis↑,
GPx4↓,
BioAv↝, WA has a rapid oral absorption and reaches to peak plasma concentration of around 16.69 ± 4.02 ng/ml within 10 min after oral administration of Withania somnifera aqueous extract at dose of 1000 mg/kg, which is equivalent to 0.458 mg/kg of WA
HSP90↓, table 1 10uM) were found to inhibit the chaperone activity of HSP90
RET↓,
E6↓,
E7↓,
Akt↓,
cMET↓,
Glycolysis↓, by suppressing the glycolysis and tricarboxylic (TCA) cycle
TCA↓,
NOTCH1↓,
STAT3↓,
AP-1↓,
PI3K↓,
eIF2α↓,
HO-1↑,
TumCCA↑, WA (1--3 uM) have been reported to inhibit cell proliferation by inducing G2 and M phase cycle arrest inovarian, breast, prostate, gastric and myelodysplastic/leukemic cancer cells and osteosarcoma
CDK1↓, WA is able to decrease the cyclin-dependent kinase 1 (Cdk1) activity and prevent Cdk1/cyclin B1 complex formation, which are key steps in cell cycle progression
*hepatoP↑, A treatment (40 mg/kg) reduces acetaminophen-induced liver injury (AILI) in mouse models and decreases H 2O 2-induced glutathione (GSH) depletion and necrosis in hepatocyte
*GSH↑,
*NRF2↑, WA triggers an anti-oxidant response after acetaminophen overdose by enhancing hepatic transcription of the nuclear factor erythroid 2–related factor 2 (NRF2)-responsive gene
Wnt↓, indirectly inhibit Wnt
EMT↓, WA can also block tumor metastasis through reduced expression of epithelial mesenchymal transition (EMT) markers.
uPA↓, WA (700 nM) exert anti-meta-static activities in breast cancer cells through inhibition of the urokinase-type plasminogen activator (uPA) protease
CSCs↓, s WA (125-500 nM) suppress tumor sphere formation indicating that the self-renewal of CSC is abolished
Nanog↓, loss of these CSC-specific characteristics is reflected in the loss of typical stem cell markers such as ALDH1A, Nanog, Sox2, CD44 and CD24
SOX2↓,
CD44↓,
lactateProd↓, drop in lactate levels compared to control mice.
Iron↑, Furthermore, we found that WA elevates the levels of intracellular labile ferrous iron (Fe +2 ) through excessive activation of heme oxygenase-1 (HMOX1), which independently causes accumulation of toxic lipid radicals and ensuing ferroptosis
NF-kB↓, nhibition of NF-kB kinase signaling pathway

473- CUR,    Curcumin inhibits epithelial-mesenchymal transition in oral cancer cells via c-Met blockade
- in-vitro, Oral, HSC4 - in-vitro, Oral, Ca9-22
Vim↓,
p‑cMET↓,
p‑ERK↓,
pro‑MMP9↓,
E-cadherin↑,

1443- Deg,    Deguelin Action Involves c-Met and EGFR Signaling Pathways in Triple Negative Breast Cancer Cells
- vitro+vivo, BC, MDA-MB-231 - in-vitro, BC, MDA-MB-435 - in-vitro, BC, BT549
EGFR↓, EGFR-PAKT/c-Met p-ERK and NF-κB by down regulating their downstream targets such as p-STAT3, c-Myc, Survivin.
Akt↓, hown to inhibit AKT activation
p‑ERK↓,
NF-kB↓,
p‑STAT3↓,
survivin↓,
Myc↓,
TumCG↓,
cMET↓,

1446- Deg,    Efficacy and mechanism of action of Deguelin in suppressing metastasis of 4T1 cells
- in-vitro, BC, 4T1
cMET↓,
p‑ERK↓,
p‑Akt↓,
TumCMig↓,
TumCG↓, vivo
Weight∅, no difference in the body weight as well as liver and spleen weights between vehicle treated control and Deguelin treated animals indicating that Deguelin was nontoxic at the dose used
*toxicity∅, no difference in the body weight as well as liver and spleen weights between vehicle treated control and Deguelin treated animals indicating that Deguelin was nontoxic at the dose used
Hif1a↓, Deguelin inhibits both ERK and p-AKT pathway leading to reduced expression of HIF −1α.
TumMeta↓,

1200- LT,    Inhibition of Fatty Acid Synthase by Luteolin Post-Transcriptionally Downregulates c-Met Expression Independent of Proteosomal/Lysosomal Degradation
- in-vitro, Pca, DU145
FASN↓, luteolin, a potent FASN inhibitor
cMET↓,
HGF/c-Met↓,

4646- OLEC,    Oleocanthal as a Multifunctional Anti-Cancer Agent: Mechanistic Insights, Advanced Delivery Strategies, and Synergies for Precision Oncology
- Review, Var, NA
BioAv↓, We provide an in-depth analysis of OC’s poor bioavailability
*Inflam↓, well-characterized anti-inflammatory and antioxidant effects
*antiOx↓,
cMET↓, inhibition of key oncogenic signaling pathways (c-MET/STAT3, PAR-2/TNF-α, COX-2/mPGES-1)
STAT3↓,
TNF-α↓,
COX2↓,
EMT↓, the suppression of epithelial-to-mesenchymal transition (EMT), angiogenesis, and metabolic reprogramming
angioG↓,
*GutMicro↝, OC’s bidirectional interaction with gut microbiota
eff↑, OC’s significant potential in combination therapies, detailing its synergistic interactions with standard treatments (e.g., PARP inhibitors, taxanes, FLT3 inhibitors)

2995- PL,    Piperlongumine overcomes osimertinib resistance via governing ubiquitination-modulated Sp1 turnover
- in-vitro, Lung, H1975 - in-vitro, Lung, PC9 - in-vivo, NA, NA
Sp1/3/4↓, piperlongumine could enhance the interaction between E3 ligase RNF4 and Sp1, inhibit the phosphorylation of Sp1 at Thr739, facilitate the ubiquitination and degradation of Sp1, lead to c-Met destabilization, and trigger intrinsic apoptosis in resista
cMET↓,
Apoptosis↑,
Cyt‑c↑, piperlongumine promoted the release of cytochrome c from the mitochondria to the cytoplasm while facilitating the translocation of Bcl-2-associated X protein (Bax) to the mitochondria
p‑ERK↓, dose-dependent decrease in the protein levels of c-Met, phosphorylated ERK1/2 (p-ERK1/2), and p-Akt
p‑Akt↓,
TumCG↓, These data suggest that piperlongumine exhibits good tolerability and effectively inhibits tumor growth of osimertinib-resistant cells in vivo.

2940- PL,    Piperlongumine Induces Reactive Oxygen Species (ROS)-dependent Downregulation of Specificity Protein Transcription Factors
- in-vitro, PC, PANC1 - in-vitro, Lung, A549 - in-vitro, Kidney, 786-O - in-vitro, BC, SkBr3
ROS↑, characterized as an inducer of reactive oxygen species (ROS)
TumCP↓, 5-15 μM piperlongumine inhibited cell proliferation and induced apoptosis and ROS,
Apoptosis↑,
eff↓, these responses were attenuated after cotreatment with the antioxidant glutathione
Sp1/3/4↓, Piperlongumine also downregulated expression of Sp1, Sp3, Sp4
cycD1/CCND1↓, and several pro-oncogenic Sp-regulated genes including cyclin D1, survivin, cMyc, epidermal growth factor receptor (EGFR) and hepatocyte growth factor receptor (cMet)
survivin↓,
cMyc↓,
EGFR↓,
cMET↓,

2948- PL,    The promising potential of piperlongumine as an emerging therapeutics for cancer
- Review, Var, NA
tumCV↓, inhibit different hallmarks of cancer such as cell survival, proliferation, invasion, angiogenesis, epithelial-mesenchymal-transition, metastases,
TumCP↓,
TumCI↓,
angioG↓,
EMT↓,
TumMeta↓,
*hepatoP↑, A study demonstrated the hepatoprotective effects of P. longum via decreasing the rate of lipid peroxidation and increasing glutathione (GSH) levels
*lipid-P↓,
*GSH↑,
cardioP↑, cardioprotective effect
CycB/CCNB1↓, downregulated the mRNA expression of the cell cycle regulatory genes such as cyclin B1, cyclin D1, cyclin-dependent kinases (CDK)-1, CDK4, CDK6, and proliferating cell nuclear antigen (PCNA)
cycD1/CCND1↓,
CDK2↓,
CDK1↓,
CDK4↓,
CDK6↓,
PCNA↓,
Akt↓, suppression of the Akt/mTOR pathway by PL was also associated with the partial inhibition of glycolysis
mTOR↓,
Glycolysis↓,
NF-kB↓, Suppression of the NF-κB signaling pathway and its related genes by PL was reported in different cancers
IKKα↓, inactivation of the inhibitor of NF-κB kinase subunit beta (IKKβ)
JAK1↓, PL efficiently inhibited cell proliferation, invasion, and migration by blocking the JAK1,2/STAT3 signaling pathway
JAK2↓,
STAT3↓,
ERK↓, PL also negatively regulates ERK1/2 signaling pathways, thereby suppressing the level of c-Fos in CRC cells
cFos↓,
Slug↓, PL was found to downregulate slug and upregulate E-cadherin and inhibited epithelial-mesenchymal transition (EMT) in breast cancer cells
E-cadherin↑,
TOP2↓, ↓topoisomerase II, ↑p53, ↑p21, ↓Bcl-2, ↑Bax, ↑Cyt C, ↑caspase-3, ↑caspase-7, ↑caspase-8
P53↑,
P21↑,
Bcl-2↓,
BAX↑,
Casp3↑,
Casp7↑,
Casp8↑,
p‑HER2/EBBR2↓, ↓p-HER1, ↓p-HER2, ↓p-HER3
HO-1↑, ↑Apoptosis, ↑HO-1, ↑Nrf2
NRF2↑,
BIM↑, ↑BIM, ↑cleaved caspase-9 and caspase-3, ↓p-FOXO3A, ↓p-Akt
p‑FOXO3↓,
Sp1/3/4↓, ↑apoptosis, ↑ROS, ↓Sp1, ↓Sp3, ↓Sp4, ↓cMyc, ↓EGFR, ↓survivin, ↓cMET
cMyc↓,
EGFR↓,
survivin↓,
cMET↓,
NQO1↑, G2/M phase arrest, ↑apoptosis, ↑ROS, ↓p-Akt, ↑Bad, ↓Bcl-2, ↑NQO1, ↑HO-1, ↑SOD2, ↑p21, ↑p-ERK, ↑p-JNK,
SOD2↑,
TrxR↓, G2/M cell cycle arrest, ↑apoptosis, ↑ROS, ↓GSH, ↓TrxR
MDM2↓, ↑ROS, ↓MDM-2, ↓cyclin B1, ↓Cdc2, G2/M phase arrest, ↑p-eIF2α, ↑ATF4, KATO III ↑CHOP, ↑apoptosis
p‑eIF2α↑,
ATF4↑,
CHOP↑,
MDA↑, ↑ROS, ↓TrxR1, ↑cleaved caspase-3, ↑CHOP, ↑MDA
Ki-67↓, ↓Ki-67, ↓MMP-9, ↓Twist,
MMP9↓,
Twist↓,
SOX2↓, ↓SOX2, ↓NANOG, ↓Oct-4, ↑E-cadherin, ↑CK18, ↓N-cadherin, ↓vimentin, ↓snail, ↓slug
Nanog↓,
OCT4↓,
N-cadherin↓,
Vim↓,
Snail↓,
TumW↓, ↓Tumor weight, ↓tumor growth
TumCG↓,
HK2↓, ↓HK2
RB1↓, ↓Rb
IL6↓, ↓IL-6, ↓IL-8,
IL8↓,
SOD1↑, ↑SOD1
RadioS↑, ombination with PL, very low intensity of radiation is found to be effective in cancer cells
ChemoSen↑, PL as a chemosensitizer which sensitized the cancer cells towards the commercially available chemotherapeutics
toxicity↓, PL does not have any adverse effect on the normal functioning of the liver and kidney.
Sp1/3/4↓, In vitro SKBR3 ↓Sp1, ↓Sp3, ↓Sp4
GSH↓, In vitro MCF-7 ↓CDK1, G2/M phase arrest ↓CDK4, ↓CDK6, ↓PCNA, ↓p-CDK1, ↑cyclin B1, ↑ROS, ↓GSH, ↓p-IκBα,
SOD↑, In vitro PANC-1, MIA PaCa-2 ↑ROS, ↑SOD1, ↑GSTP1, ↑HO-1

89- QC,  doxoR,    Quercetin reverses the doxorubicin resistance of prostate cancer cells by downregulating the expression of c-met
- in-vitro, Pca, PC3
PI3K/Akt↓, quercetin targeted c-met to inhibit the PI3K/AKT pathway in doxorubicin-resistant prostate cancer cells.
cMET↓, quercetin treatment significantly inhibited c-met expression in PC3/R cells
Casp3↑, combination treatment with quercetin to induce expression of cleaved caspase-3 and −9
Casp9↑,
MMP↓, combination treatment with quercetin and doxorubicin induced a significant decrease of MMP in PC3/R cells compared with cells treated with doxorubicin alone.
ChemoSen↑, Quercetin increased the sensitivity of PC3/R cells to doxorubicin
ROS↑, ROS, which are considered to be key apoptotic inducers (17) were released from the mitochondria into the cytoplasm, due to MMP collapse induced by co-treatment with quercetin and doxorubicin

3427- TQ,    Chemopreventive and Anticancer Effects of Thymoquinone: Cellular and Molecular Targets
ROS⇅, It appears that the cellular and/or physiological context(s) determines whether TQ acts as a pro-oxidant or an anti-ox- idant in vivo
Fas↑, Figure 2, cell death
DR5↑,
TRAIL↑,
Casp3↑,
Casp8↑,
Casp9↑,
P53↑,
mTOR↓,
Bcl-2↓,
BID↓,
CXCR4↓,
JNK↑,
p38↑,
MAPK↑,
LC3II↑,
ATG7↑,
Beclin-1↑,
AMPK↑,
PPARγ↑, cell survival
eIF2α↓,
P70S6K↓,
VEGF↓,
ERK↓,
NF-kB↓,
XIAP↓,
survivin↓,
p65↓,
DLC1↑, epigenetic
FOXO↑,
TET2↑,
CYP1B1↑,
UHRF1↓,
DNMT1↓,
HDAC1↓,
IL2↑, inflammation
IL1↓,
IL6↓,
IL10↓,
IL12↓,
TNF-α↓,
iNOS↓,
COX2↓,
5LO↓,
AP-1↓,
PI3K↓, invastion
Akt↓,
cMET↓,
VEGFR2↓,
CXCL1↓,
ITGA5↓,
Wnt↓,
β-catenin/ZEB1↓,
GSK‐3β↓,
Myc↓,
cycD1/CCND1↓,
N-cadherin↓,
Snail↓,
Slug↓,
Vim↓,
Twist↓,
Zeb1↓,
MMP2↓,
MMP7↓,
MMP9↓,
JAK2↓, cell proliferiation
STAT3↓,
NOTCH↓,
cycA1/CCNA1↓,
CDK2↓,
CDK4↓,
CDK6↓,
CDC2↓,
CDC25↓,
Mcl-1↓,
E2Fs↓,
p16↑,
p27↑,
P21↑,
ChemoSen↑, Such chemo-potentiating effects of TQ in different cancer cells have been observed with 5-fluorouracil in gastric cancer and colorectal cancer models


Showing Research Papers: 1 to 13 of 13

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 13

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Ferroptosis↑, 2,   GPx4↓, 1,   GSH↓, 1,   HO-1↑, 2,   Iron↑, 1,   MDA↑, 1,   NQO1↑, 1,   NRF2↑, 1,   ROS↑, 4,   ROS⇅, 1,   SOD↑, 1,   SOD1↑, 1,   SOD2↑, 1,   TrxR↓, 1,  

Mitochondria & Bioenergetics ⓘ

CDC2↓, 1,   CDC25↓, 1,   MMP↓, 1,   XIAP↓, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 1,   ATG7↑, 1,   cMyc↓, 3,   FASN↓, 1,   Glycolysis↓, 2,   HK2↓, 1,   lactateProd↓, 1,   PI3K/Akt↓, 1,   PPARγ↑, 1,   TCA↓, 1,  

Cell Death ⓘ

Akt↓, 6,   p‑Akt↓, 2,   Apoptosis↑, 4,   BAX↑, 2,   Bcl-2↓, 2,   BID↓, 1,   BIM↑, 2,   Casp3↑, 3,   Casp7↑, 1,   Casp8↑, 2,   Casp9↑, 2,   p‑Chk2↑, 1,   Cyt‑c↑, 1,   DR5↑, 2,   Fas↑, 1,   Ferroptosis↑, 2,   HGF/c-Met↓, 1,   iNOS↓, 1,   JNK↑, 1,   MAPK↑, 2,   Mcl-1↓, 1,   MDM2↓, 1,   Myc↓, 2,   oncosis↑, 1,   p27↑, 2,   p38↑, 2,   survivin↓, 5,   TRAIL↑, 1,  

Kinase & Signal Transduction ⓘ

p‑HER2/EBBR2↓, 1,   RET↓, 1,   Sp1/3/4↓, 4,  

Transcription & Epigenetics ⓘ

tumCV↓, 1,  

Protein Folding & ER Stress ⓘ

CHOP↑, 2,   eIF2α↓, 2,   p‑eIF2α↑, 1,   HSP90↓, 1,  

Autophagy & Lysosomes ⓘ

Beclin-1↑, 1,   LC3II↑, 1,   TumAuto↑, 1,  

DNA Damage & Repair ⓘ

p‑ATM↑, 1,   p‑ATR↑, 1,   p‑CHK1↑, 1,   CYP1B1↑, 1,   DNAdam↑, 1,   DNMT1↓, 1,   HR↓, 1,   p16↑, 2,   P53↑, 2,   PCNA↓, 1,   RAD51↓, 1,   UHRF1↓, 1,  

Cell Cycle & Senescence ⓘ

CDK1↓, 2,   CDK2↓, 2,   CDK4↓, 2,   cycA1/CCNA1↓, 1,   CycB/CCNB1↓, 1,   cycD1/CCND1↓, 4,   cycE1↓, 1,   E2Fs↓, 1,   P21↑, 2,   RB1↓, 1,   TumCCA↑, 2,  

Proliferation, Differentiation & Cell State ⓘ

CD44↓, 1,   cFos↓, 1,   cMET↓, 12,   p‑cMET↓, 1,   CSCs↓, 1,   EMT↓, 3,   ERK↓, 3,   p‑ERK↓, 4,   FOXO↑, 1,   p‑FOXO3↓, 1,   GSK‐3β↓, 1,   HDAC1↓, 1,   mTOR↓, 3,   Nanog↓, 3,   NOTCH↓, 1,   NOTCH1↓, 1,   OCT4↓, 1,   P70S6K↓, 1,   PI3K↓, 3,   SOX2↓, 3,   STAT3↓, 4,   p‑STAT3↓, 1,   TOP2↓, 1,   TumCG↓, 4,   Wnt↓, 2,   Wnt/(β-catenin)↓, 1,  

Migration ⓘ

5LO↓, 1,   AP-1↓, 2,   CDK4/6↓, 1,   DLC1↑, 1,   E-cadherin↑, 2,   ITGA5↓, 1,   ITGB1↑, 1,   Ki-67↓, 1,   MMP2↓, 2,   MMP7↓, 1,   MMP9↓, 2,   pro‑MMP9↓, 1,   N-cadherin↓, 2,   NCAM↑, 1,   Slug↓, 2,   Snail↓, 2,   TGF-β↓, 1,   TIMP2↑, 1,   TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 2,   TumMeta↓, 2,   Twist↓, 2,   uPA↓, 1,   Vim↓, 3,   Zeb1↓, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 2,   ATF4↑, 1,   EGFR↓, 4,   Hif1a↓, 2,   KDR/FLK-1↓, 1,   NO↓, 1,   VEGF↓, 2,   VEGFR2↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 2,   CXCL1↓, 1,   CXCR4↓, 1,   IKKα↓, 1,   IL1↓, 2,   IL10↓, 1,   IL12↓, 1,   IL2↑, 1,   IL6↓, 3,   IL8↓, 1,   JAK1↓, 1,   JAK2↓, 2,   MIP2↓, 1,   NF-kB↓, 5,   p65↓, 1,   PGE2↓, 1,   TNF-α↓, 3,  

Hormonal & Nuclear Receptors ⓘ

CDK6↓, 2,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   BioAv↝, 1,   ChemoSen↑, 3,   eff↓, 1,   eff↑, 1,   RadioS↑, 1,   TET2↑, 1,  

Clinical Biomarkers ⓘ

E6↓, 1,   E7↓, 1,   EGFR↓, 4,   p‑HER2/EBBR2↓, 1,   IL6↓, 3,   Ki-67↓, 1,   Myc↓, 2,  

Functional Outcomes ⓘ

cardioP↑, 1,   toxicity↓, 1,   TumW↓, 1,   Weight∅, 1,  
Total Targets: 187

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↓, 1,   GSH↑, 2,   lipid-P↓, 1,   NRF2↑, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,  

Clinical Biomarkers ⓘ

GutMicro↝, 1,  

Functional Outcomes ⓘ

hepatoP↑, 2,   toxicity∅, 1,  
Total Targets: 8

Scientific Paper Hit Count for: cMET, cellular hepatocyte growth factor receptor
3 Piperlongumine
2 Deguelin
1 Apigenin (mainly Parsley)
1 Artemisinin
1 Ashwagandha(Withaferin A)
1 Curcumin
1 Luteolin
1 Oleocanthal
1 Quercetin
1 doxorubicin
1 Thymoquinone
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#:484  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

 

Home Page