Quercetin / Casp3 Cancer Research Results

QC, Quercetin: Click to Expand ⟱
Features:
Plant pigment (flavonoid) found in red wine, onions, green tea, apples and berries.
Quercetin is thought to contribute to anticancer effects through several mechanisms:
-Antioxidant Activity:
-Induction of Apoptosis:modify Bax:Bcl-2 ratio
-Anti-inflammatory Effects:
-Cell Cycle Arrest:
-Inhibition of Angiogenesis and Metastasis: (VEGF)

Cellular Pathways:
-PI3K/Akt/mTOR Pathway: central to cell proliferation, survival, and metabolism.
-MAPK/ERK Pathway: influencing cell proliferation, differentiation, and apoptosis.
-NF-κB Pathway: downregulate NF-κB
-JAK/STAT Pathway: interfere with the activation of STAT3
-Apoptotic Pathways: intrinsic (mitochondrial) and extrinsic (death receptor-mediated) pathways

Quercetin has been used at doses around 500–1000 mg per day
Quercetin’s bioavailability from foods or standard supplements can be low.

-Note half-life 11 to 28 hours.
BioAv low 1-10%, poor water-solubility, consuming with fat may improve bioavialability. also piperine or VitC.
Pathways:
- induce ROS production in cancer cells (higher dose). Typicallys Lowers ROS in normal cells(unless it is high dose?)or depends on Redox status?. "quercetin paradox"
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, UPR↑, GRP78↑, Ca+2↑, Cyt‑c↑, Caspases↑, DNA damage↑, cl-PARP↑, HSP↓, Prx,
- Confusing info about Lowering AntiOxidant defense in Cancer Cells: NRF2↓(some contrary), TrxR↓**, SOD↓(contrary), GSH↓ Catalase↓(contrary), HO1↓(some contrary), GPx↓(some contrary)
- Raises AntiOxidant defense in Normal Cells: ROS↓, NRF2↑, SOD↑, GSH↑, Catalase↑,
- lowers Inflammation : NF-kB↓, COX2↓, p38↓, Pro-Inflammatory Cytokines : NLRP3↓, IL-1β↓, TNF-α↓, IL-6↓, IL-8↓
- inhibit Growth/Metastases : TumMeta↓, TumCG↓, EMT↓, MMPs↓, MMP2↓, MMP9↓, TIMP2, IGF-1↓, uPA↓, VEGF↓, ROCK1↓, FAK↓, NF-κB↓, CXCR4↓, SDF1↓, TGF-β↓, α-SMA↓, ERK↓
- reactivate genes thereby inhibiting cancer cell growth : HDAC↓, DNMTs↓, EZH2↓, P53↑, HSP↓, Sp proteins↓, TET↑
- cause Cell cycle arrest : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓,
- inhibits Migration/Invasion : TumCMig↓, TumCI↓, TNF-α↓, FAK↓, ERK↓, EMT↓, TOP1↓, TET1,
- inhibits glycolysis and ATP depletion : HIF-1α↓, PKM2↓, cMyc↓, GLUT1↓, LDH↓, LDHA↓, HK2↓, PFKs↓, PDKs↓, ECAR↓, OXPHOS↓, GRP78↑, GlucoseCon↓
- inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, Notch↓, FGF↓, PDGF↓, EGFR↓,
- some indication of inhibiting Cancer Stem Cells : CSC↓, CK2↓, Hh↓, CD24↓, β-catenin↓, Notch2↓,
- Others: PI3K↓, AKT↓, JAK↓, STAT↓, Wnt↓, β-catenin↓, AMPK, α↓, ERK↓, JNK, - SREBP (related to cholesterol).
- Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, RadioProtective, Others(review target notes), Neuroprotective, Cognitive, Renoprotection, Hepatoprotective, CardioProtective,

- Selectivity: Cancer Cells vs Normal Cells

Rank Pathway / Axis Cancer Cells Normal Cells Label Primary Interpretation Notes
1 Reactive oxygen species (ROS) ↑ ROS (dose-, metal-, context-dependent) ↓ ROS Conditional Driver Biphasic redox modulation Quercetin exhibits pro-oxidant behavior in cancer cells while protecting normal cells
2 Mitochondrial integrity / intrinsic apoptosis ↓ ΔΨm; ↑ caspase activation ↔ preserved Driver Execution of intrinsic apoptosis Mitochondrial dysfunction is a central apoptosis route in cancer cells
3 PI3K → AKT → mTOR axis ↓ AKT / ↓ mTOR ↔ adaptive suppression Driver Growth and survival inhibition AKT/mTOR suppression is a consistently reported upstream effect in cancer models
4 NF-κB signaling ↓ NF-κB activation ↓ inflammatory NF-κB tone Secondary Reduced survival and inflammatory transcription NF-κB inhibition contributes to chemosensitization and apoptosis susceptibility
5 MAPK signaling (JNK / p38) ↑ JNK / ↑ p38 ↔ minimal Secondary Stress-mediated apoptosis signaling MAPK activation supports apoptosis downstream of redox stress
6 Cell cycle regulation ↑ G1/S or G2/M arrest ↔ largely spared Phenotypic Cytostatic growth control Cell-cycle arrest reflects disruption of growth signaling
7 HIF-1α hypoxia signaling ↓ HIF-1α ↔ minimal Secondary Reduced hypoxia tolerance Quercetin interferes with hypoxia-driven transcriptional programs
8 NRF2 antioxidant response ↑ NRF2 (adaptive, context-dependent) ↑ NRF2 (protective) Adaptive Stress compensation NRF2 induction reflects redox buffering rather than primary cytotoxicity


Casp3, CPP32, Cysteinyl aspartate specific proteinase-3: Click to Expand ⟱
Source:
Type:
Also known as CP32.
Cysteinyl aspartate specific proteinase-3 (Caspase-3) is a common key protein in the apoptosis and pyroptosis pathways, and when activated, the expression level of tumor suppressor gene Gasdermin E (GSDME) determines the mechanism of tumor cell death.
As a key protein of apoptosis, caspase-3 can also cleave GSDME and induce pyroptosis. Loss of caspase activity is an important cause of tumor progression.
Many anticancer strategies rely on the promotion of apoptosis in cancer cells as a means to shrink tumors. Crucial for apoptotic function are executioner caspases, most notably caspase-3, that proteolyze a variety of proteins, inducing cell death. Paradoxically, overexpression of procaspase-3 (PC-3), the low-activity zymogen precursor to caspase-3, has been reported in a variety of cancer types. Until recently, this counterintuitive overexpression of a pro-apoptotic protein in cancer has been puzzling. Recent studies suggest subapoptotic caspase-3 activity may promote oncogenic transformation, a possible explanation for the enigmatic overexpression of PC-3. Herein, the overexpression of PC-3 in cancer and its mechanistic basis is reviewed; collectively, the data suggest the potential for exploitation of PC-3 overexpression with PC-3 activators as a targeted anticancer strategy.
Caspase 3 is the main effector caspase and has a key role in apoptosis. In many types of cancer, including breast, lung, and colon cancer, caspase-3 expression is reduced or absent.
On the other hand, some studies have shown that high levels of caspase-3 expression can be associated with a better prognosis in certain types of cancer, such as breast cancer. This suggests that caspase-3 may play a role in the elimination of cancer cells, and that therapies aimed at activating caspase-3 may be effective in treating certain types of cancer.
Procaspase-3 is a apoptotic marker protein.
Prognostic significance:
• High Cas3 expression: Associated with good prognosis and increased sensitivity to chemotherapy in breast, gastric, lung, and pancreatic cancers.
• Low Cas3 expression: Linked to poor prognosis and increased risk of recurrence in colorectal, hepatocellular carcinoma, ovarian, and prostate cancers.
Scientific Papers found: Click to Expand⟱
910- QC,    The Anti-Cancer Effect of Quercetin: Molecular Implications in Cancer Metabolism
tumCV↓, Apoptosis↑, PI3k/Akt/mTOR↓, Wnt/(β-catenin)↓, MAPK↝, ERK↝, TumCCA↑, H2O2↑, ROS↑, TumAuto↑, MMPs↓, P53↑, Casp3↑, Hif1a↓, cFLIP↓, IL6↓, IL10↓, lactateProd↓, Glycolysis↓, PKM2↓, GLUT1↓, COX2↓, VEGF↓, OCR↓, ECAR↓, STAT3↓, MMP2↓, MMP9:TIMP1↓, mTOR↓,
923- QC,    Quercetin as an innovative therapeutic tool for cancer chemoprevention: Molecular mechanisms and implications in human health
- Review, Var, NA
ROS↑, GSH↓, Ca+2↝, MMP↓, Casp3↑, Casp8↑, Casp9↑, other↓, *ROS↓, *NRF2↑, HO-1↑, TumCCA↑, Inflam↓, STAT3↓, DR5↑, P450↓, MMPs↓, IFN-γ↓, IL6↓, COX2↓, IL8↓, iNOS↓, TNF-α↓, cl‑PARP↑, Apoptosis↑, P53↑, Sp1/3/4↓, survivin↓, TRAILR↑, Casp10↑, DFF45↑, TNFR 1↑, Fas↑, NF-kB↓, IKKα↓, cycD1/CCND1↓, Bcl-2↓, BAX↑, PI3K↓, Akt↓, E-cadherin↓, Vim↓, β-catenin/ZEB1↓, cMyc↓, EMT↓, MMP2↓, NOTCH1↓, MMP7↓, angioG↓, TSP-1↑, CSCs↓, XIAP↓, Snail↓, Slug↓, LEF1↓, P-gp↓, EGFR↓, GSK‐3β↓, mTOR↓, RAGE↓, HSP27↓, VEGF↓, TGF-β↓, COL1↓, COL3A1↓,
914- QC,    Quercetin and Cancer Chemoprevention
- Review, NA, NA
GSH↓, ROS↑, TumCCA↑, Ca+2↑, MMP↓, Casp3↑, Casp8↑, Casp9↑, β-catenin/ZEB1↓, AMPKα↑, ASK1↑, p38↑, TRAIL↑, DR5↑, cFLIP↓, Apoptosis↑,
60- QC,  EGCG,  isoFl,    The dietary bioflavonoid quercetin synergizes with epigallocathechin gallate (EGCG) to inhibit prostate cancer stem cell characteristics, invasion, migration and epithelial-mesenchymal transition
- in-vitro, Pca, pCSCs
Casp3↑, Casp7↑, Bcl-2↓, survivin↓, XIAP↓, EMT↓, Slug↓, Snail↓, β-catenin/ZEB1↓, LEF1↓, CSCs↓, Apoptosis↑, TumCMig↓, TumCI↓, CD44↓, CD133↓,
55- QC,    Quercetin inhibits the growth of human gastric cancer stem cells by inducing mitochondrial-dependent apoptosis through the inhibition of PI3K/Akt signaling
- in-vitro, GC, GCSCs
Bcl-2↓, BAX↑, Cyt‑c↑, MMP↓, PI3K/Akt↓, Casp3↑, Casp9↑, TumCG↓, Apoptosis↑, CSCs↓,
64- QC,    Quercetin enhances TRAIL-mediated apoptosis in colon cancer cells by inducing the accumulation of death receptors in lipid rafts
- in-vitro, Colon, HT-29 - in-vitro, Colon, SW-620 - in-vitro, Colon, Caco-2
Cyt‑c↑, BAX↑, Casp3↑, DR4↑, DR5↑,
66- QC,    Emerging impact of quercetin in the treatment of prostate cancer
- Review, Pca, NA
CycB/CCNB1↓, CDK1↓, EMT↓, PI3K↓, MAPK↓, Wnt/(β-catenin)↓, PSA↓, VEGF↓, PARP↑, Casp3↑, Casp9↑, DR5↑, ROS⇅, Shh↓, P53↑, P21↑, EGFR↓, TumCCA↑, ROS↑, miR-21↓, TumCP↓, selectivity↑, PDGF↓, EGF↓, TNF-α↓, VEGFR2↓, mTOR↓, cMyc↓, MMPs↓, GRP78/BiP↑, CHOP↑,
36- QC,    Quercetin induces G2 phase arrest and apoptosis with the activation of p53 in an E6 expression-independent manner in HPV-positive human cervical cancer-derived cells
- in-vitro, Cerv, HeLa - in-vitro, Cerv, SiHa
P53↑, P21↑, BAX↑, Casp3↑, Casp7↑, TumCCA↑, ROS↑, TumCCA↑, Apoptosis↑,
41- QC,    Quercetin induces mitochondrial-derived apoptosis via reactive oxygen species-mediated ERK activation in HL-60 leukemia cells and xenograft
- vitro+vivo, AML, HL-60
Casp8↑, Casp9↑, Casp3↑, ROS↑, ERK↑, cl‑PARP↑, MMP↓, eff↓,
42- QC,    Quercetin induces apoptosis by activating caspase-3 and regulating Bcl-2 and cyclooxygenase-2 pathways in human HL-60 cells
- in-vitro, AML, HL-60
Bcl-2↓, BAX↑, Casp3↑, COX2↓,
50- QC,    Anticancer effect and mechanism of polymer micelle-encapsulated quercetin on ovarian cancer
- vitro+vivo, Ovarian, A2780S
Casp3↑, Casp9↑, Mcl-1↓, Bcl-2↓, BAX↑, angioG↓, TumCG↓, Apoptosis↑, p‑p44↓, Akt↓, TumCP↓, eff↑,
86- QC,  PacT,    Quercetin regulates insulin like growth factor signaling and induces intrinsic and extrinsic pathway mediated apoptosis in androgen independent prostate cancer cells (PC-3)
- vitro+vivo, Pca, PC3
BAD↑, IGFBP3↑, Cyt‑c↑, cl‑Casp9↑, Casp10↑, cl‑PARP↑, Casp3↑, IGF-1R↓, PI3K↓, p‑Akt↓, cycD1/CCND1↓, IGF-1↓, IGF-2↓, IGF-1R↓, MMP↓, Apoptosis↑, NA?,
93- QC,    Chemical Proteomics Identifies Heterogeneous Nuclear Ribonucleoprotein (hnRNP) A1 as the Molecular Target of Quercetin in Its Anti-cancer Effects in PC-3 Cells
- in-vitro, Pca, PC3
hnRNPA1↓, Casp3↑, Casp7↑, TumCD↑, IAP1↓,
91- QC,    The roles of endoplasmic reticulum stress and mitochondrial apoptotic signaling pathway in quercetin-mediated cell death of human prostate cancer PC-3 cells
- in-vitro, Pca, PC3
CDK2↓, cycE/CCNE↓, cycD1/CCND1↓, ATFs↑, GRP78/BiP↑, Bcl-2↓, BAX↑, Casp3↑, Casp8↑, Casp9↑, ER Stress↑, CHOP↑, TumCCA↑, DNAdam↑, AIF↑, Ca+2↑, MMP↓,
90- QC,  HP,    Combination of quercetin and hyperoside inhibits prostate cancer cell growth and metastasis via regulation of microRNA‑21
- in-vitro, Pca, PC3
ROS↑, cl‑Casp3↑, cl‑PARP↑, miR-21↓, PDCD4↑, TAC↑, tumCV↓, TumCI↓,
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↓, cMET↓, Casp3↑, Casp9↑, MMP↓, ChemoSen↑, ROS↑,
69- QC,    Quercetin enhances TRAIL-induced apoptosis in prostate cancer cells via increased protein stability of death receptor 5
- in-vitro, Pca, DU145 - in-vitro, Pca, PC3 - in-vitro, Pca, LNCaP
TRAIL↑, Casp3↑, Casp9↑, Casp8↑, DR5↑,
84- QC,    Quercetin-induced growth inhibition and cell death in prostatic carcinoma cells (PC-3) are associated with increase in p21 and hypophosphorylated retinoblastoma proteins expression
- in-vitro, Pca, PC3
P21↑, cDC2↓, CDK1↓, CycB/CCNB1↓, Casp3↑, Bcl-2↓, Bcl-xL↓, BAX↑, pRB↓, TumCCA↑, Apoptosis↑,
73- QC,    The dietary bioflavonoid, quercetin, selectively induces apoptosis of prostate cancer cells by down-regulating the expression of heat shock protein 90
- in-vitro, Pca, LNCaP - in-vitro, Pca, DU145 - in-vitro, Pca, PC3
HSP90↓, Casp3↑, Casp9↑, TumCG↓, TumCD↑, selectivity↑, toxicity↓,
77- QC,  EGCG,    The dietary bioflavonoid quercetin synergizes with epigallocathechin gallate (EGCG) to inhibit prostate cancer stem cell characteristics, invasion, migration and epithelial-mesenchymal transition
- in-vitro, Pca, CD44+ - in-vitro, NA, CD133+ - in-vitro, NA, PC3 - in-vitro, NA, LNCaP
Casp3↑, Casp7↑, Bcl-2↓, survivin↓, XIAP↓, EMT↓, Vim↓, Slug↓, Snail↓, β-catenin/ZEB1↓, LEF1↓, TCF↓, eff↑, CSCs↓, TumCG↓, tumCV↓,
78- QC,    Effects of quercetin on insulin-like growth factors (IGFs) and their binding protein-3 (IGFBP-3) secretion and induction of apoptosis in human prostate cancer cells
- in-vitro, Pca, PC3
IGF-1↓, IGF-2↓, IGFBP3↑, Bcl-2↓, Bcl-xL↓, Casp3↑, Apoptosis↑, BAX↑, DNAdam↑,
79- QC,    Chemopreventive Effect of Quercetin in MNU and Testosterone Induced Prostate Cancer of Sprague-Dawley Rats
- in-vivo, Pca, NA
GSH↑, SOD↑, Catalase↑, GPx↑, GSR↑, IGF-1R↓, Akt↓, AR↓, TumCP↓, lipid-P↓, H2O2↓, Raf↓, p‑MEK↓, Bcl-2↑, Bcl-xL↑, Casp3↑, Casp8↑, Casp9↑,
3603- QC,    Mechanism of quercetin therapeutic targets for Alzheimer disease and type 2 diabetes mellitus
- Review, AD, NA - Review, Diabetic, NA
*MAPK↓, *neuroP↑, *ROS↓, *Akt↓, *PI3K↓, *IL6↓, *TNF-α↓, *VEGF↓, *EGFR↓, *Casp3↓, *Bcl-2↓, *IL1β↓,
4787- QC,    Quercetin: A Phytochemical with Pro-Apoptotic Effects in Colon Cancer Cells
- Review, CRC, NA
Inflam↓, AntiCan↑, Apoptosis↑, MMP↓, P53↑, BAX↑, Casp3↑, Casp9↑, Bcl-2↓, NF-kB↓, IL6↓, IL1β↓, *antiOx↑, *lipid-P↓, *ROS↓, MAPK↓, JAK↓, STAT↓, PI3K↓, Akt↓, chemoP↑, ROS⇅, DNAdam↑, ChemoSen↝,
4827- QC,  CUR,    Synthetic Pathways and the Therapeutic Potential of Quercetin and Curcumin
- Review, Var, NA
*AntiCan↑, *Inflam↓, *Bacteria↓, *AntiDiabetic↑, *ROS↓, *SOD↑, *Catalase↑, *GSH↑, *NRF2↑, *Trx↑, *IronCh↑, *MDA↑, cycD1/CCND1↓, PI3K↓, Casp3↑, BAX↑, ChemoSen↑, ROS↑, eff↑, MMP↓, Cyt‑c↑, Akt↓, ERK↓,
3353- QC,    Quercetin triggers cell apoptosis-associated ROS-mediated cell death and induces S and G2/M-phase cell cycle arrest in KON oral cancer cells
- in-vitro, Oral, KON - in-vitro, Nor, MRC-5
tumCV↓, selectivity↑, TumCCA↑, TumCMig↓, TumCI↓, Apoptosis↑, TumMeta↓, Bcl-2↓, BAX↑, TIMP1↑, MMP2↓, MMP9↓, *Inflam↓, *neuroP↑, *cardioP↑, p38↓, MAPK↓, Twist↓, P21↓, cycD1/CCND1↓, Casp3↑, Casp9↑, p‑Akt↓, p‑ERK↓, CD44↓, CD24↓, ChemoSen↑, MMP↓, Cyt‑c↑, AIF↑, ROS↑, Ca+2↑, Hif1a↓, VEGF↓,
3350- QC,    Quercetin and the mitochondria: A mechanistic view
- Review, NA, NA
*antiOx↑, *Inflam↓, *NRF2↑, ROS⇅, *NRF2↑, *HO-1↑, *PPARα↑, *PGC-1α↑, *SIRT1↑, *ATP↑, ATP↓, ERK↓, cl‑PARP↑, Casp9↑, Casp8↑, BAX↑, MMP↓, Cyt‑c↑, Casp3↑, HSP27↓, HSP72↓, RAS↓, Raf↓,
3373- QC,    The Effect of Quercetin in the Yishen Tongluo Jiedu Recipe on the Development of Prostate Cancer through the Akt1-related CXCL12/ CXCR4 Pathway
- in-vitro, Pca, DU145
TumCP↓, Casp3↑, Bcl-2↓, Apoptosis↑, TumCI↓, TumCMig↓, CXCL12↓, CXCR4↓,
3371- QC,    Quercetin induces MGMT+ glioblastoma cells apoptosis via dual inhibition of Wnt3a/β-Catenin and Akt/NF-κB signaling pathways
- in-vitro, GBM, T98G
TIMP2↑, TumCG↓, TumCMig↓, Apoptosis↑, TumCCA↑, MMP↓, ROS↑, Bax:Bcl2↑, cl‑Casp9↑, cl‑Casp3↑, DNAdam↑, γH2AX↑, MGMT↓, cl‑PARP↑,
3369- QC,    Pharmacological basis and new insights of quercetin action in respect to its anti-cancer effects
- Review, Pca, NA
FAK↓, TumCCA↑, p‑pRB↓, CDK2↑, CycB/CCNB1↓, CDK1↓, EMT↓, PI3K↓, MAPK↓, Wnt↓, ROS↑, miR-21↑, Akt↓, NF-kB↓, FasL↑, Bak↑, BAX↑, Bcl-2↓, Casp3↓, Casp9↑, P53↑, p38↑, MAPK↑, Cyt‑c↑, PARP↓, CHOP↑, ROS↓, LDH↑, GRP78/BiP↑, ERK↑, MDA↓, SOD↑, GSH↑, NRF2↑, VEGF↓, PDGF↓, EGF↓, FGF↓, TNF-α↓, TGF-β↓, VEGFR2↓, EGFR↓, FGFR1↓, mTOR↓, cMyc↓, MMPs↓, LC3B-II↑, Beclin-1↑, IL1β↓, CRP↓, IL10↓, COX2↓, IL6↓, TLR4↓, Shh↓, HER2/EBBR2↓, NOTCH↓, DR5↑, HSP70/HSPA5↓, CSCs↓, angioG↓, MMP2↓, MMP9↓, IGFBP3↑, uPA↓, uPAR↓, RAS↓, Raf↓, TSP-1↑,
3368- QC,    The potential anti-cancer effects of quercetin on blood, prostate and lung cancers: An update
- Review, Var, NA
*Inflam↓, *antiOx↑, *AntiCan↑, Casp3↓, p‑Akt↓, p‑mTOR↓, p‑ERK↓, β-catenin/ZEB1↓, Hif1a↓, AntiAg↓, VEGFR2↓, EMT↓, EGFR↓, MMP2↓, MMP↓, TumMeta↓, MMPs↓, Akt↓, Snail↓, N-cadherin↓, Vim↓, E-cadherin↑, STAT3↓, TGF-β↓, ROS↓, P53↑, BAX↑, PKCδ↓, PI3K↓, COX2↓, cFLIP↓, cycD1/CCND1↓, cMyc↓, IL6↓, IL10↓, Cyt‑c↑, TumCCA↑, DNMTs↓, HDAC↓, ac‑H3↑, ac‑H4↑, Diablo↑, Casp3↑, Casp9↑, PARP1↑, eff↑, PTEN↑, VEGF↓, NO↓, iNOS↓, ChemoSen↑, eff↑, eff↑, eff↑, uPA↓, CXCR4↓, CXCL12↓, CLDN2↓, CDK6↓, MMP9↓, TSP-1↑, Ki-67↓, PCNA↓, ROS↑, ER Stress↑,
3362- QC,    The effect of quercetin on cervical cancer cells as determined by inducing tumor endoplasmic reticulum stress and apoptosis and its mechanism of action
- in-vitro, Cerv, HeLa
Apoptosis↑, cycD1/CCND1↓, Casp3↑, GRP78/BiP↑, CHOP↑, tumCV↓, IRE1↑, p‑PERK↑, c-ATF6↑, ER Stress↑,
104- RES,  QC,    Resveratrol and Quercetin in Combination Have Anticancer Activity in Colon Cancer Cells and Repress Oncogenic microRNA-27a
- in-vitro, Colon, HT-29
Casp3↑, PARP↑, survivin↓, miR-27a-3p↓, Sp1/3/4↓, ZBTB10↑, ROS⇅, TAC↑, tumCV↓,

Showing Research Papers: 1 to 33 of 33

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 33

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned ⓘ

NA?, 1,  

Redox & Oxidative Stress ⓘ

Catalase↑, 1,   GPx↑, 1,   GSH↓, 2,   GSH↑, 2,   GSR↑, 1,   H2O2↓, 1,   H2O2↑, 1,   HO-1↑, 1,   lipid-P↓, 1,   MDA↓, 1,   NRF2↑, 1,   ROS↓, 2,   ROS↑, 13,   ROS⇅, 4,   SOD↑, 2,   TAC↑, 2,  

Mitochondria & Bioenergetics ⓘ

AIF↑, 2,   ATP↓, 1,   EGF↓, 2,   FGFR1↓, 1,   p‑MEK↓, 1,   MMP↓, 13,   OCR↓, 1,   Raf↓, 3,   XIAP↓, 3,  

Core Metabolism/Glycolysis ⓘ

cMyc↓, 4,   ECAR↓, 1,   Glycolysis↓, 1,   lactateProd↓, 1,   LDH↑, 1,   PI3K/Akt↓, 2,   PI3k/Akt/mTOR↓, 1,   PKM2↓, 1,  

Cell Death ⓘ

Akt↓, 7,   p‑Akt↓, 3,   Apoptosis↑, 15,   ASK1↑, 1,   BAD↑, 1,   Bak↑, 1,   BAX↑, 15,   Bax:Bcl2↑, 1,   Bcl-2↓, 13,   Bcl-2↑, 1,   Bcl-xL↓, 2,   Bcl-xL↑, 1,   Casp10↑, 2,   Casp3↓, 2,   Casp3↑, 29,   cl‑Casp3↑, 2,   Casp7↑, 4,   Casp8↑, 7,   Casp9↑, 16,   cl‑Casp9↑, 2,   cFLIP↓, 3,   Cyt‑c↑, 8,   Diablo↑, 1,   DR4↑, 1,   DR5↑, 6,   Fas↑, 1,   FasL↑, 1,   IAP1↓, 1,   iNOS↓, 2,   MAPK↓, 4,   MAPK↑, 1,   MAPK↝, 1,   Mcl-1↓, 1,   p38↓, 1,   p38↑, 2,   PDCD4↑, 1,   survivin↓, 4,   TNFR 1↑, 1,   TRAIL↑, 2,   TRAILR↑, 1,   TumCD↑, 2,  

Kinase & Signal Transduction ⓘ

AMPKα↑, 1,   HER2/EBBR2↓, 1,   Sp1/3/4↓, 2,  

Transcription & Epigenetics ⓘ

ac‑H3↑, 1,   ac‑H4↑, 1,   miR-21↓, 2,   miR-21↑, 1,   miR-27a-3p↓, 1,   other↓, 1,   pRB↓, 1,   p‑pRB↓, 1,   tumCV↓, 6,  

Protein Folding & ER Stress ⓘ

c-ATF6↑, 1,   ATFs↑, 1,   CHOP↑, 4,   ER Stress↑, 3,   GRP78/BiP↑, 4,   HSP27↓, 2,   HSP70/HSPA5↓, 1,   HSP72↓, 1,   HSP90↓, 1,   IRE1↑, 1,   p‑PERK↑, 1,  

Autophagy & Lysosomes ⓘ

Beclin-1↑, 1,   LC3B-II↑, 1,   TumAuto↑, 1,  

DNA Damage & Repair ⓘ

DFF45↑, 1,   DNAdam↑, 4,   DNMTs↓, 1,   MGMT↓, 1,   P53↑, 7,   PARP↓, 1,   PARP↑, 2,   cl‑PARP↑, 6,   PARP1↑, 1,   PCNA↓, 1,   γH2AX↑, 1,  

Cell Cycle & Senescence ⓘ

CDK1↓, 3,   CDK2↓, 1,   CDK2↑, 1,   CycB/CCNB1↓, 3,   cycD1/CCND1↓, 7,   cycE/CCNE↓, 1,   P21↓, 1,   P21↑, 3,   TumCCA↑, 12,  

Proliferation, Differentiation & Cell State ⓘ

CD133↓, 1,   CD24↓, 1,   CD44↓, 2,   cDC2↓, 1,   cMET↓, 1,   CSCs↓, 5,   EMT↓, 6,   ERK↓, 2,   ERK↑, 2,   ERK↝, 1,   p‑ERK↓, 2,   FGF↓, 1,   GSK‐3β↓, 1,   HDAC↓, 1,   IGF-1↓, 2,   IGF-1R↓, 3,   IGF-2↓, 2,   IGFBP3↑, 3,   mTOR↓, 4,   p‑mTOR↓, 1,   NOTCH↓, 1,   NOTCH1↓, 1,   PI3K↓, 7,   PTEN↑, 1,   RAS↓, 2,   Shh↓, 2,   STAT↓, 1,   STAT3↓, 3,   TCF↓, 1,   TumCG↓, 5,   Wnt↓, 1,   Wnt/(β-catenin)↓, 2,  

Migration ⓘ

AntiAg↓, 1,   Ca+2↑, 3,   Ca+2↝, 1,   CLDN2↓, 1,   COL1↓, 1,   COL3A1↓, 1,   CXCL12↓, 2,   E-cadherin↓, 1,   E-cadherin↑, 1,   FAK↓, 1,   hnRNPA1↓, 1,   Ki-67↓, 1,   LEF1↓, 3,   MMP2↓, 5,   MMP7↓, 1,   MMP9↓, 3,   MMP9:TIMP1↓, 1,   MMPs↓, 5,   N-cadherin↓, 1,   p‑p44↓, 1,   PDGF↓, 2,   PKCδ↓, 1,   RAGE↓, 1,   Slug↓, 3,   Snail↓, 4,   TGF-β↓, 3,   TIMP1↑, 1,   TIMP2↑, 1,   TSP-1↑, 3,   TumCI↓, 4,   TumCMig↓, 4,   TumCP↓, 4,   TumMeta↓, 2,   Twist↓, 1,   uPA↓, 2,   uPAR↓, 1,   Vim↓, 3,   β-catenin/ZEB1↓, 5,  

Angiogenesis & Vasculature ⓘ

angioG↓, 3,   EGFR↓, 4,   Hif1a↓, 3,   NO↓, 1,   VEGF↓, 6,   VEGFR2↓, 3,   ZBTB10↑, 1,  

Barriers & Transport ⓘ

GLUT1↓, 1,   P-gp↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 5,   CRP↓, 1,   CXCR4↓, 2,   IFN-γ↓, 1,   IKKα↓, 1,   IL10↓, 3,   IL1β↓, 2,   IL6↓, 5,   IL8↓, 1,   Inflam↓, 2,   JAK↓, 1,   NF-kB↓, 3,   PSA↓, 1,   TLR4↓, 1,   TNF-α↓, 3,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,   CDK6↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 4,   ChemoSen↝, 1,   eff↓, 1,   eff↑, 7,   P450↓, 1,   selectivity↑, 3,  

Clinical Biomarkers ⓘ

AR↓, 1,   CRP↓, 1,   EGFR↓, 4,   HER2/EBBR2↓, 1,   IL6↓, 5,   Ki-67↓, 1,   LDH↑, 1,   PSA↓, 1,   RAGE↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   chemoP↑, 1,   toxicity↓, 1,  
Total Targets: 235

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 3,   Catalase↑, 1,   GSH↑, 1,   HO-1↑, 1,   lipid-P↓, 1,   MDA↑, 1,   NRF2↑, 4,   ROS↓, 4,   SOD↑, 1,   Trx↑, 1,  

Metal & Cofactor Biology ⓘ

IronCh↑, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↑, 1,   PGC-1α↑, 1,  

Core Metabolism/Glycolysis ⓘ

PPARα↑, 1,   SIRT1↑, 1,  

Cell Death ⓘ

Akt↓, 1,   Bcl-2↓, 1,   Casp3↓, 1,   MAPK↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

PI3K↓, 1,  

Angiogenesis & Vasculature ⓘ

EGFR↓, 1,   VEGF↓, 1,  

Immune & Inflammatory Signaling ⓘ

IL1β↓, 1,   IL6↓, 1,   Inflam↓, 4,   TNF-α↓, 1,  

Clinical Biomarkers ⓘ

EGFR↓, 1,   IL6↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 2,   AntiDiabetic↑, 1,   cardioP↑, 1,   neuroP↑, 2,  

Infection & Microbiome ⓘ

Bacteria↓, 1,  
Total Targets: 33

Scientific Paper Hit Count for: Casp3, CPP32, Cysteinyl aspartate specific proteinase-3
33 Quercetin
2 EGCG (Epigallocatechin Gallate)
1 isoflavones
1 Paclitaxel
1 Hyperoside
1 doxorubicin
1 Curcumin
1 Resveratrol
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#:140  Target#:42  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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