Quercetin / Akt 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.
EMIQ bioavialability is about 3X that of Quercetin (Example Natural Factors brand)
Isoquercitrin is high bioaviability and efficiacy but at this time does not seem available as supplement.

-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


Akt, PKB-Protein kinase B: Click to Expand ⟱
Source: HalifaxProj(inhibit)
Type:
Akt1 is involved in cellular survival pathways, by inhibiting apoptotic processes; Akt2 is an important signaling molecule in the insulin signaling pathway. It is required to induce glucose transport.

Inhibitors:
-Curcumin: downregulate AKT phosphorylation and signaling.
-Resveratrol
-Quercetin: inhibit the PI3K/AKT pathway.
-Epigallocatechin Gallate (EGCG)
-Luteolin and Apigenin: inhibit AKT phosphorylation


Scientific Papers found: Click to Expand⟱
2342- QC,    Quercetin Inhibits the Proliferation of Glycolysis-Addicted HCC Cells by Reducing Hexokinase 2 and Akt-mTOR Pathway
- in-vitro, HCC, Bel-7402 - in-vitro, HCC, SMMC-7721 cell - in-vivo, NA, NA
TumCP↓, HK2↓, Akt↓, mTOR↓, GlucoseCon↓, lactateProd↓, Glycolysis↓,
2341- QC,    Quercetin suppresses the mobility of breast cancer by suppressing glycolysis through Akt-mTOR pathway mediated autophagy induction
- in-vitro, BC, MCF7 - in-vitro, BC, MDA-MB-231 - in-vivo, NA, NA
MMP2↓, MMP9↓, VEGF↓, Glycolysis↓, lactateProd↓, PKM2↓, GLUT1↓, LDHA↓, TumAuto↑, Akt↓, mTOR↓, TumMeta↓, MMP3↓, eff↓, GlucoseCon↓, lactateProd↓, TumAuto↑, LC3B-II↑,
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/PTGS2↓, 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/ABCB1↓, EGFR↓, GSK‐3β↓, mTOR↓, RAGE↓, HSP27↓, VEGF↓, TGF-β↓, COL1↓, COL3A1↓,
916- QC,    Quercetin and cancer: new insights into its therapeutic effects on ovarian cancer cells
- Review, Ovarian, NA
COX2/PTGS2↓, CRP↓, ER Stress↑, Apoptosis↑, GRP78/BiP↑, CHOP/DDIT3↑, p‑STAT3↓, PI3K↓, Akt↓, mTOR↓, cMyc↓, cycD1/CCND1↓, cFLIP↓, IL6↓, IL10↓,
54- QC,    Quercetin‑3‑methyl ether suppresses human breast cancer stem cell formation by inhibiting the Notch1 and PI3K/Akt signaling pathways
- in-vitro, BC, MCF7
EMT↓, E-cadherin↑, Vim↓, MMP2↓, NOTCH1↓, PI3K/Akt↓, PI3k/Akt/mTOR↓, p‑Akt↓, EZH2↓, H3K27ac↓, TumCCA↑, CSCs↓, CDK1↓, CycB/CCNB1↓, Bcl-xL↓, Bcl-2↓, Nanog↓, H3↓,
61- QC,    Midkine downregulation increases the efficacy of quercetin on prostate cancer stem cell survival and migration through PI3K/AKT and MAPK/ERK pathway
- in-vitro, Pca, PC3 - in-vitro, Pca, LNCaP - in-vitro, Pca, ARPE-19
p‑PI3K↓, p‑Akt↓, p‑ERK↓, NF-kB↓, p38↓, ABCG2↓, CD44↓, CD133↓, CSCs↓,
63- QC,    Quercetin facilitates cell death and chemosensitivity through RAGE/PI3K/AKT/mTOR axis in human pancreatic cancer cells
- in-vitro, Pca, NA
RAGE↓, PI3K↓, mTOR↓, Akt↓, Apoptosis↑, TumAuto↑, ChemoSen↑,
39- QC,    A Comprehensive Analysis and Anti-Cancer Activities of Quercetin in ROS-Mediated Cancer and Cancer Stem Cells
- Analysis, NA, NA
ROS↑, GSH↓, IL6↓, COX2/PTGS2↓, IL8↓, iNOS↓, TNF-α↓, MAPK↑, ERK↑, SOD↑, ATP↓, Casp↑, PI3K/Akt↓, mTOR↓, NOTCH1↓, Bcl-2↓, BAX↑, IFN-γ↓, TumCP↓, TumCCA↑, Akt↓, P70S6K↓, *Keap1↓, *GPx↑, *Catalase↑, *HO-1↑, *NRF2↑, NRF2↑, eff↑, HIF-1↓,
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?,
95- QC,    Quercetin, a natural dietary flavonoid, acts as a chemopreventive agent
- in-vitro, Pca, PC3
p‑ERK↓, p‑STAT3↓, p‑Akt↓, N-cadherin↓, Vim↓, cycD1/CCND1↓, Snail↓, Slug↓, Twist↓, PCNA↓, EGFR↓, chemoPv↑,
92- QC,    Quercetin Inhibits Angiogenesis Mediated Human Prostate Tumor Growth by Targeting VEGFR- 2 Regulated AKT/mTOR/P70S6K Signaling Pathways
- vitro+vivo, Pca, HUVECs - vitro+vivo, Pca, PC3
VEGFR2/KDR/Flk1↓, HemoG↓, Akt↓, mTOR↓, P70S6K↓, angioG↓,
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↑,
80- QC,    Quercetin reverses EGF-induced epithelial to mesenchymal transition and invasiveness in prostate cancer (PC-3) cell line via EGFR/PI3K/Akt pathway
- in-vitro, Pca, PC3
Vim↓, ERK↓, Snail↓, Slug↓, Twist↓, EGFR↓, p‑Akt↓, EGFR↓, N-cadherin↓, TumMeta↓, EMT↓,
81- QC,  EGCG,    Enhanced inhibition of prostate cancer xenograft tumor growth by combining quercetin and green tea
- in-vivo, Pca, NA
COMT↓, MRP1/ABCC1↓, Ki-67↓, Bax:Bcl2↑, AR↓, Akt↓, p‑ERK↓, COMT↓, eff↑, chemoPv↑, BioAv↑,
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↓,
3354- QC,    Quercetin: Its Main Pharmacological Activity and Potential Application in Clinical Medicine
- Review, Var, NA
*ROS↓, *IronCh↓, *lipid-P↓, *GSH↑, *NRF2↑, TumCCA↑, ER Stress↑, P53↑, CDK2↓, cycA1/CCNA1↓, CycB/CCNB1↓, cycE/CCNE↓, cycD1/CCND1↓, PCNA↓, P21↑, p27/CDKN1B↑, PI3K↓, Akt↓, mTOR↓, STAT3↓, cFLIP↓, cMyc↓, survivin↓, DR5↓, *Inflam↓, *IL6↓, *IL8↓, COX2/PTGS2↓, 5LO↓, *cardioP↑, *FASN↓, *AntiAg↑, *MDA↓,
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↓,
3341- QC,    Antioxidant Activities of Quercetin and Its Complexes for Medicinal Application
- Review, Var, NA - Review, Stroke, NA
*antiOx↑, *BioAv↑, *GSH↑, *AChE↓, *BChE↓, *H2O2↓, *lipid-P↓, *SOD↑, *SOD2↑, *Catalase↑, *GPx↑, *neuroP↑, *HO-1↑, *cardioP↑, *MDA↓, *NF-kB↓, *IKKα↓, *ROS↓, *PI3K↑, *Akt↑, *hepatoP↑, P53↑, BAX↑, IGF-1R↓, Akt↓, AR↓, TumCP↓, GSH↑, SOD↑, Catalase↑, lipid-P↓, *TNF-α↓, *Ca+2↓,
3378- QC,    CK2 and PI3K are direct molecular targets of quercetin in chronic lymphocytic leukaemia
- in-vitro, AML, NA
CK2↓, PI3K↓, TumCD↑, Akt↓, Mcl-1↓, PTEN↑,
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/DDIT3↑, ROS↓, LDH↑, GRP78/BiP↑, ERK↑, MDA↓, SOD↑, GSH↑, NRF2↑, VEGF↓, PDGF↓, EGF↓, FGF↓, TNF-α↓, TGF-β↓, VEGFR2/KDR/Flk1↓, EGFR↓, FGFR1↓, mTOR↓, cMyc↓, MMPs↓, LC3B-II↑, Beclin-1↑, IL1β↓, CRP↓, IL10↓, COX2/PTGS2↓, 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/KDR/Flk1↓, EMT↓, EGFR↓, MMP2↓, MMP↓, TumMeta↓, MMPs↓, Akt↓, Snail↓, N-cadherin↓, Vim↓, E-cadherin↑, STAT3↓, TGF-β↓, ROS↓, P53↑, BAX↑, PKCδ↓, PI3K↓, COX2/PTGS2↓, 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↑,

Showing Research Papers: 1 to 24 of 24

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 24

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0)

NA?, 1,  

Redox & Oxidative Stress(tgid=1)

Catalase↑, 2,   GPx↑, 1,   GSH↓, 2,   GSH↑, 3,   GSR↑, 1,   H2O2↓, 1,   HO-1↑, 1,   lipid-P↓, 2,   MDA↓, 1,   NRF2↑, 2,   ROS↓, 2,   ROS↑, 6,   ROS⇅, 1,   SOD↑, 4,  

Mitochondria & Bioenergetics(tgid=3)

AIF↑, 1,   ATP↓, 1,   EGF↓, 1,   FGFR1↓, 1,   p‑MEK↓, 1,   MMP↓, 6,   Raf↓, 2,   XIAP↓, 1,  

Core Metabolism/Glycolysis(tgid=4)

cMyc↓, 5,   GlucoseCon↓, 2,   Glycolysis↓, 2,   HK2↓, 1,   lactateProd↓, 3,   LDH↑, 1,   LDHA↓, 1,   PI3K/Akt↓, 2,   PI3k/Akt/mTOR↓, 1,   PKM2↓, 1,  

Cell Death(tgid=5)

Akt↓, 17,   p‑Akt↓, 7,   Apoptosis↑, 7,   BAD↑, 1,   Bak↑, 1,   BAX↑, 9,   Bax:Bcl2↑, 1,   Bcl-2↓, 7,   Bcl-2↑, 1,   Bcl-xL↓, 1,   Bcl-xL↑, 1,   Casp↑, 1,   Casp10↑, 2,   Casp3↓, 2,   Casp3↑, 8,   Casp8↑, 2,   Casp9↑, 7,   cl‑Casp9↑, 1,   cFLIP↓, 3,   CK2↓, 1,   Cyt‑c↑, 5,   Diablo↑, 1,   DR5↓, 1,   DR5↑, 2,   Fas↑, 1,   FasL↑, 1,   iNOS↓, 3,   MAPK↓, 3,   MAPK↑, 2,   Mcl-1↓, 2,   p27/CDKN1B↑, 1,   p38↓, 2,   p38↑, 1,   survivin↓, 2,   TNFR 1↑, 1,   TRAILR↑, 1,   TumCD↑, 1,  

Kinase & Signal Transduction(tgid=6)

HER2/EBBR2↓, 1,   Sp1/3/4↓, 1,  

Transcription & Epigenetics(tgid=7)

EZH2↓, 1,   H3↓, 1,   ac‑H3↑, 1,   ac‑H4↑, 1,   miR-21↑, 1,   other↓, 1,   p‑pRB↓, 1,   tumCV↓, 1,  

Protein Folding & ER Stress(tgid=8)

CHOP/DDIT3↑, 2,   ER Stress↑, 3,   GRP78/BiP↑, 2,   HSP27↓, 1,   HSP70/HSPA5↓, 1,  

Autophagy & Lysosomes(tgid=9)

Beclin-1↑, 1,   LC3B-II↑, 2,   TumAuto↑, 3,  

DNA Damage & Repair(tgid=10)

DFF45↑, 1,   DNAdam↑, 1,   DNMTs↓, 1,   P53↑, 6,   PARP↓, 1,   cl‑PARP↑, 2,   PARP1↑, 1,   PCNA↓, 3,  

Cell Cycle & Senescence(tgid=11)

CDK1↓, 2,   CDK2↓, 1,   CDK2↑, 1,   cycA1/CCNA1↓, 1,   CycB/CCNB1↓, 3,   cycD1/CCND1↓, 8,   cycE/CCNE↓, 1,   P21↓, 1,   P21↑, 1,   TumCCA↑, 7,  

Proliferation, Differentiation & Cell State(tgid=12)

CD133↓, 1,   CD24↓, 1,   CD44↓, 2,   CSCs↓, 4,   EMT↓, 5,   ERK↓, 2,   ERK↑, 2,   p‑ERK↓, 5,   FGF↓, 1,   GSK‐3β↓, 1,   H3K27ac↓, 1,   HDAC↓, 1,   IGF-1↓, 1,   IGF-1R↓, 4,   IGF-2↓, 1,   IGFBP3↑, 2,   mTOR↓, 9,   p‑mTOR↓, 1,   Nanog↓, 1,   NOTCH↓, 1,   NOTCH1↓, 3,   P70S6K↓, 2,   PI3K↓, 10,   p‑PI3K↓, 1,   PTEN↑, 2,   RAS↓, 1,   Shh↓, 1,   STAT↓, 1,   STAT3↓, 3,   p‑STAT3↓, 2,   TumCG↓, 1,   Wnt↓, 1,  

Migration(tgid=13)

5LO↓, 1,   AntiAg↓, 1,   Ca+2↑, 1,   Ca+2↝, 1,   CLDN2↓, 1,   COL1↓, 1,   COL3A1↓, 1,   CXCL12↓, 1,   E-cadherin↓, 1,   E-cadherin↑, 2,   FAK↓, 1,   Ki-67↓, 2,   LEF1↓, 1,   MMP2↓, 6,   MMP3↓, 1,   MMP7↓, 1,   MMP9↓, 4,   MMPs↓, 3,   N-cadherin↓, 3,   p‑p44↓, 1,   PDGF↓, 1,   PKCδ↓, 1,   RAGE↓, 2,   Slug↓, 3,   Snail↓, 4,   TGF-β↓, 3,   TIMP1↑, 1,   TSP-1↑, 3,   TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 5,   TumMeta↓, 4,   Twist↓, 3,   uPA↓, 2,   uPAR↓, 1,   Vim↓, 5,   β-catenin/ZEB1↓, 2,  

Angiogenesis & Vasculature(tgid=14)

angioG↓, 4,   EGFR↓, 6,   HIF-1↓, 1,   Hif1a↓, 2,   NO↓, 1,   VEGF↓, 5,   VEGFR2/KDR/Flk1↓, 3,  

Barriers & Transport(tgid=15)

GLUT1↓, 1,   P-gp/ABCB1↓, 1,  

Immune & Inflammatory Signaling(tgid=16)

COX2/PTGS2↓, 6,   CRP↓, 2,   CXCR4↓, 1,   IFN-γ↓, 2,   IKKα↓, 1,   IL10↓, 3,   IL1β↓, 2,   IL6↓, 6,   IL8↓, 2,   Inflam↓, 2,   JAK↓, 1,   NF-kB↓, 4,   TLR4↓, 1,   TNF-α↓, 3,  

Hormonal & Nuclear Receptors(tgid=20)

AR↓, 3,   CDK6↓, 1,   COMT↓, 2,  

Drug Metabolism & Resistance(tgid=21)

ABCG2↓, 1,   BioAv↑, 1,   ChemoSen↑, 4,   ChemoSen↝, 1,   eff↓, 1,   eff↑, 8,   MRP1/ABCC1↓, 1,   P450↓, 1,   selectivity↑, 1,  

Clinical Biomarkers(tgid=22)

AR↓, 3,   CRP↓, 2,   EGFR↓, 6,   EZH2↓, 1,   HemoG↓, 1,   HER2/EBBR2↓, 1,   IL6↓, 6,   Ki-67↓, 2,   LDH↑, 1,   RAGE↓, 2,  

Functional Outcomes(tgid=23)

AntiCan↑, 1,   chemoP↑, 1,   chemoPv↑, 2,  
Total Targets: 223

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1)

antiOx↑, 3,   Catalase↑, 3,   GPx↑, 2,   GSH↑, 3,   H2O2↓, 1,   HO-1↑, 2,   Keap1↓, 1,   lipid-P↓, 3,   MDA↓, 2,   MDA↑, 1,   NRF2↑, 4,   ROS↓, 6,   SOD↑, 2,   SOD2↑, 1,   Trx↑, 1,  

Metal & Cofactor Biology(tgid=2)

IronCh↓, 1,   IronCh↑, 1,  

Core Metabolism/Glycolysis(tgid=4)

FASN↓, 1,  

Cell Death(tgid=5)

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

Proliferation, Differentiation & Cell State(tgid=12)

PI3K↓, 1,   PI3K↑, 1,  

Migration(tgid=13)

AntiAg↑, 1,   Ca+2↓, 1,  

Angiogenesis & Vasculature(tgid=14)

EGFR↓, 1,   VEGF↓, 1,  

Immune & Inflammatory Signaling(tgid=16)

IKKα↓, 1,   IL1β↓, 1,   IL6↓, 2,   IL8↓, 1,   Inflam↓, 4,   NF-kB↓, 1,   TNF-α↓, 2,  

Synaptic & Neurotransmission(tgid=18)

AChE↓, 1,   BChE↓, 1,  

Drug Metabolism & Resistance(tgid=21)

BioAv↑, 1,  

Clinical Biomarkers(tgid=22)

EGFR↓, 1,   IL6↓, 2,  

Functional Outcomes(tgid=23)

AntiCan↑, 2,   AntiDiabetic↑, 1,   cardioP↑, 3,   hepatoP↑, 1,   neuroP↑, 3,  

Infection & Microbiome(tgid=24)

Bacteria↓, 1,  
Total Targets: 47

Scientific Paper Hit Count for: Akt, PKB-Protein kinase B
24 Quercetin
1 Paclitaxel/Taxol
1 EGCG (Epigallocatechin Gallate)
1 Curcumin
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#:4  State#:%  Dir#:1
wNotes=0 sortOrder:rid,rpid

 

Home Page