PI3K/Akt Cancer Research Results

PI3K/Akt, PI3K/Akt signaling: Click to Expand ⟱
Source: HalifaxProj(inhibit) TCGA
Type:
The PI3K/Akt signaling pathway plays a crucial role in various cellular processes, including growth, proliferation, survival, and metabolism.
Pathway Components:
Phosphoinositide 3-kinases (PI3Ks): A family of enzymes that phosphorylate the inositol ring of phosphatidylinositol, leading to the production of phosphatidylinositol (3,4,5)-trisphosphate (PIP3).
Akt (Protein Kinase B): A serine/threonine kinase that is activated by PIP3. Once activated, Akt phosphorylates various substrates involved in cell survival and growth.
Overactivation can lead to uncontrolled cell growth.
Angiogenesis: Akt can promote the expression of pro-angiogenic factors, facilitating the formation of new blood vessels to supply tumors with nutrients and oxygen.
Scientific Papers found: Click to Expand⟱
247- AL,    Allicin inhibits the invasion of lung adenocarcinoma cells by altering tissue inhibitor of metalloproteinase/matrix metalloproteinase balance via reducing the activity of phosphoinositide 3-kinase/AKT signaling
- in-vitro, Lung, A549 - in-vitro, Lung, H1299
MMP2↓, protein levels of
MMP9↓, protein levels of
TIMP1↑,
TIMP2↑,
p‑Akt↓,
PI3K/Akt↓,

583- Api,  Cisplatin,    Apigenin suppresses GLUT-1 and p-AKT expression to enhance the chemosensitivity to cisplatin of laryngeal carcinoma Hep-2 cells: an in vitro study
- in-vitro, Laryn, HEp2
PI3K/Akt↓,
GLUT1↓,
Akt↓,

206- Api,    Inhibition of glutamine utilization sensitizes lung cancer cells to apigenin-induced apoptosis resulting from metabolic and oxidative stress
- in-vitro, Lung, H1299 - in-vitro, Lung, H460 - in-vitro, Lung, A549 - in-vitro, CRC, HCT116 - in-vitro, Melanoma, A375 - in-vitro, Lung, H2030 - in-vitro, CRC, SW480
Glycolysis↓, glucose consumption, lactate production, and ATP production were all strongly decreased by apigenin
lactateProd↓,
PGK1↓,
ALDOA↓,
GLUT1↓, Apigenin reduces GLUT1 expression levels.
ENO1↓,
ATP↓,
Casp9↑,
Casp3↑,
cl‑PARP↑, cleavage
PI3K/Akt↓,
HK1↓, HK1, HK2
HK2↓,
ROS↑, Apigenin causes oxidative stress leading to apoptosis. Because apoptotic signal transduction cascades involving caspase-9, -3 and PARP cleavage can be activated by increased ROS levels
Apoptosis↑,
eff↓, Cancer cells expressing high levels of GLUT1 are resistant to apigenin-induced apoptosis through metabolic compensation of glucose utilization.
NADPH↓, apigenin significantly decreased glucose utilization through suppression of GLUT1 expression, and consequently decreased NADPH production, which led to increased ROS levels.
PPP↓, inhibition of the PPP

171- Api,    Apigenin in cancer therapy: anti-cancer effects and mechanisms of action
- Review, Var, NA
PI3K/Akt↓,
NF-kB↓,
CK2↓,
FOXO↓,
MAPK↝, modulation of MAPKs by apigenin contributed to apigenin-induced cell cycle arrest at G0/G1 phase
ERK↓, p-ERK1/2,
p‑JAK↓, phosphorylation
Wnt/(β-catenin)↓,
ROS↑, accumulation of reactive oxygen species (ROS) production, leading to induction of DNA damage
CDC25↓,
p‑STAT↓,
DNAdam↑,

147- ATG,  EGCG,  CUR,    Increased chemopreventive effect by combining arctigenin, green tea polyphenol and curcumin in prostate and breast cancer cells
- in-vitro, Pca, LNCaP - in-vitro, Pca, MCF-7
Bax:Bcl2↑, combination treatment significantly increased the ratio of Bax to Bcl-2 proteins, decreased the activation of NFκB, PI3K/Akt and Stat3
NF-kB↓, arctigenin demonstrated the strongest ability to inhibit the activation of both PI3K/Akt and NFκB pathways in both LNCaP and MCF-7 cells.
PI3K/Akt↓,
STAT3↓,
chemoPv↑, combining Arc and EGCG with Cur to enhance chemoprevention in both prostate and breast cancer.
TumCP↓, combining Arc and EGCG with Cur to enhance chemoprevention in both prostate and breast cancer.
TumCCA↑, EGCG significantly increased the effect of curcumin on cell cycle arrest at G0/G1 phase in MCF-7 cells, and the effect was further enhanced by the addition of arctigenin
TumCMig↓, EGCG and arctigenin alone or in combination with curcumin significantly decreased the number of migrated MCF-7 cells compared to control

136- CUR,  docx,    Combinatorial effect of curcumin with docetaxel modulates apoptotic and cell survival molecules in prostate cancer
- in-vitro, Pca, DU145 - in-vitro, Pca, PC3
Bcl-2↓, combined treatment with curcumin with docetaxel down-regulates the expression of the anti-apoptotic proteins BCL-2, BCL-XL and MCL-1 in DU145 and PC3 cells
Bcl-xL↓,
Mcl-1↓,
BAX↑, Whereas, the expression of the pro-apoptotic markers BAK and BID were significantly up-regulated in curcumin with docetaxel treated group compared to curcumin and docetaxel-treated group alone
BID↑,
PARP↑, combined treatment with curcumin and docetaxel in DU145 and PC3 cells enhanced proteolysis of PARP compared
NF-kB↓, Curcumin blocks NF-κB activation in docetaxel-treated PCa cells
CDK1↓, treatment of curcumin and docetaxel significantly reduced the expression of the proliferation marker CDK-1 and inflammatory marker COX-2
COX2↓,
RTK-RAS↓,
PI3K/Akt↓, combined treatment of curcumin and docetaxel reduced the expression of PI3K, phospho-AKT, EGFR and HER2 in both DU145 and PC3 cells
EGFR↓,
HER2/EBBR2↓, docetaxel in combination with curcumin down-regulates the expression of HER2 and EGFR resulting inhibition of the expression of PI3K kinase and phospho-AKT
P53↑,
ChemoSen↑, The combined treatment of curcumin and docetaxel inhibited the proliferation and induced apoptosis significantly higher than the curcumin and docetaxel-treated group alone.

1442- Deg,    Deguelin, a novel anti-tumorigenic agent targeting apoptosis, cell cycle arrest and anti-angiogenesis for cancer chemoprevention
- Review, Var, NA
PI3K/Akt↓, Deguelin is a well-known PI3K/Akt inhibitor
IKKα↓,
AMP↓,
mTOR↓,
survivin↓,
NF-kB↓,
Apoptosis↑,
TumCCA↑, G1-S phase cell cycle arrest
toxicity↓, No sign of overt toxicity has been observed at the dose of 2–4 mg/kg
HSP90↓,
Casp↑, caspase cascade of apoptosis is initiated
TumCG↓,
p27↑, found to regulate cell cycle in colon cancer cells by stimulating p27
cycE/CCNE↓,
angioG↓,
Hif1a↓,
VEGF↓,
*toxicity↑, Treatment with deguelin, a potential mitochondria complex I inhibitor (34), reduced tyrosine hydroxylase-positive neurons, leading to Parkinson’s disease (PD).

19- Deg,    Deguelin inhibits proliferation and migration of human pancreatic cancer cells in vitro targeting hedgehog pathway
- in-vitro, PC, Bxpc-3 - in-vitro, PC, PANC1
HH↓, The activation of the hedgehog (Hh) signaling pathway, as well as matrix metalloproteinases (MMP)-2 and MMP-9, was suppressed by deguelin.
Gli1↓,
PTCH1↓,
Sufu↓,
MMP2↓, Deguelin downregulates MMP-2 and MMP-9 in Bxpc-3 and Panc-1 cells
MMP9↓,
PI3K/Akt↓,
HIF-1↓,
VEGF↓,
IKKα↓,
NF-kB↓,
EMT↓,
AMPK↑,
mTOR↓,
survivin↓,
TumCG↓, Deguelin treatment was observed to inhibit growth and induce apoptosis in two PC cell lines (Bxpc-3 and Panc-1)
Apoptosis↑,
TumCMig↓, Deguelin inhibits migration and invasion of PC cells
TumCI↓,

668- EGCG,    The Potential Role of Epigallocatechin-3-Gallate (EGCG) in Breast Cancer Treatment
- Review, BC, MCF-7 - Review, BC, MDA-MB-231
HER2/EBBR2↓,
EGFR↓,
mtDam↑,
ROS↑,
PI3K/Akt↓,
P53↑,
P21↑,
Casp3↑,
Casp9↑,
BAX↑,
PTEN↑,
Bcl-2↓,
hTERT/TERT↓,
STAT3↓,
TumCCA↑, EGCG causes cell cycle arrest by preventing cyclin accumulation D1
Hif1a↓,

682- EGCG,    Suppressive Effects of EGCG on Cervical Cancer
- Review, NA, NA
E7↓,
E6↓,
PI3K/Akt↓,
P53↑,
p27↑,
P21↑,
CDK2↓,
mTOR↓,
HIF-1↓,
IGF-1↓,
EGFR↓,
ERK↓, ERK1/2
VEGF↓,

805- GAR,  Cisplatin,  PacT,    Garcinol Exhibits Anti-Neoplastic Effects by Targeting Diverse Oncogenic Factors in Tumor Cells
- Review, NA, NA
ERK↓, ERK1/2
PI3K/Akt↓,
Wnt/(β-catenin)↓,
STAT3↓,
NF-kB↓,
ChemoSen↑, cisplatin or paclitaxel, in the presence of garcinol can lead to a significant increase in the treatment outcome
COX2↓,
Casp3↑,
Casp9↑,
BAX↑,
Bcl-2↓,
VEGF↓,
TGF-β↓,
HATs↓,
E-cadherin↑,
Vim↓,
Zeb1↓,
ZEB2↓,
Let-7↑,
MMP9↓,
TumCCA↑, cycle arrest at G0/G1 phase
ROS↑,
MMP↓,
IL6↓,
NOTCH1↓,

802- GAR,    Garcinol acts as an antineoplastic agent in human gastric cancer by inhibiting the PI3K/AKT signaling pathway
- in-vitro, GC, HGC27
TumCP↓,
TumCI↓,
Apoptosis↑,
PI3K/Akt↓, garcinol may inhibit gastric tumorigenesis by suppressing the PI3K/AKT signaling pathway
Akt↓, inhibited the levels of AKTp-Thr308 and AKTp-ser473
p‑mTOR↓, while the expression of total mTOR remained stable
cycD1/CCND1↓,
MMP2↓,
MMP9↓,
BAX↑,
Bcl-2↓,

830- GAR,    Garcinol modulates tyrosine phosphorylation of FAK and subsequently induces apoptosis through down-regulation of Src, ERK, and Akt survival signaling in human colon cancer cells
- in-vitro, CRC, HT-29
TumCI↓,
TumCMig↓,
Apoptosis↑,
p‑FAK↓,
Src↓,
MAPK↓,
ERK↓,
PI3K/Akt↓,
Bax:Bcl2↑,
Cyt‑c↑, release of cytochrome c from the mitochondria to the cytosol
MMP7↓,

834- Gra,    Anticancer Properties of Graviola (Annona muricata): A Comprehensive Mechanistic Review
- Review, NA, NA
EGFR↓,
PI3K/Akt↓,
NF-kB↓,
JAK↓,
STAT↓,
Hif1a↓, inhibition of HIF-1α, GLUT1, and GLUT4 [
GLUT1↓,
GLUT4↓,
ROS↑, generation of reactive oxygen species (ROS) via upregulatoin of enzyme systems like catalase (CAT), superoxide dismutase (SOD), and heme-oxygenase (HO-1) expression
Catalase↑,
SOD↑,
HO-1↑,

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↑, upregulation of Cyt-c following treatment with quercetin
MMP↓, quercetin-induced apoptosis occurred via the mitochondrial-dependent pathway, which was mediated via the PI3K-Akt pathway.
PI3K/Akt↓,
Casp3↑,
Casp9↑,
TumCG↓, quercetin has the potential to effectively intervene and prevent GCSC growth
Apoptosis↑,
CSCs↓, Quercetin inhibits the growth of human gastric cancer stem cells

71- QC,    Role of Bax in quercetin-induced apoptosis in human prostate cancer cells
- in-vitro, Pca, LNCaP - in-vitro, Pca, PrEC - in-vitro, Pca, YPEN-1 - in-vitro, Pca, HCT116
Casp8↑, quercetin inhibits the PI3K/Akt pathway, suppresses phosphorylation of Bad, and subsequently alters interaction between Bcl-xL and Bax in human prostate carcinoma LNCaP cells
Casp9↑,
PARP↑,
BAD↓,
BAX↑,
PI3K/Akt↓, quercetin inhibits the PI3K/Akt pathway, suppresses phosphorylation of Bad, and subsequently alters interaction between Bcl-xL and Bax in human prostate carcinoma LNCaP cells
Cyt‑c↑, accompanied by cytochrome c release, and procaspases-3, -8 and -9 cleavage and increased poly (ADP-ribose) polymerase (PARP) cleavage.
selectivity↑, quercetin treatment did not affect the viability or rate of apoptosis in normal human prostate epithelial cell line (PrEC)

39- QC,    A Comprehensive Analysis and Anti-Cancer Activities of Quercetin in ROS-Mediated Cancer and Cancer Stem Cells
- Analysis, NA, NA
ROS↑, production of ROS in both cancer, and cancer stem cells,
GSH↓, By directly reducing the intracellular pool of glutathione (GSH), QC can influence ROS metabolism
IL6↓, QC is its ability to inhibit inflammatory mediators including IFN-γ, IL-6, COX-2, IL-8, iNOS, TNF-α, and many other cancer inflammatory mechanisms
COX2↓,
IL8↓,
iNOS↓,
TNF-α↓,
MAPK↑, quercetin-3-methyl ether stopped the growth of cancer in the esophagus by blocking the Akt/mTOR/P70S6k and MAPK pathways, which are important for the growth of cancer
ERK↑,
SOD↑,
ATP↓,
Casp↑,
PI3K/Akt↓,
mTOR↓,
NOTCH1↓,
Bcl-2↓,
BAX↑,
IFN-γ↓,
TumCP↓, QC directly involves inducing apoptosis and/or the cell cycle arrest process, and also inhibits the propagation of rapidly proliferating cells
TumCCA↑,
Akt↓, quercetin-3-methyl ether stopped the growth of cancer in the esophagus by blocking the Akt/mTOR/P70S6k and MAPK pathways, which are important for the growth of cancer
P70S6K↓,
*Keap1↓,
*GPx↑, inhibiting its negative regulator, Keap1, resulting in Nrf-2 nuclear translocation [86]. This results in the production and activation of enzymes namely GPX, CAT, heme oxygenase 1 (HO-1), peroxiredoxin (PRX)
*Catalase↑,
*HO-1↑,
*NRF2↑,
NRF2↑, The effect of QC on nuclear translocation of Nrf-2 in a time-dependent manner, and increased expression level in HepG2, MgM (malignant mesothelioma) MSTO-211H, and H2452 cells at mRNA and protein quantity has been reported recently
eff↑, quercetin coupled with gold nanoparticles promoted apoptosis by inhibiting the EGFR/P13K/Akt-mediated pathway
HIF-1↓, Quercetin has been shown to suppress the Akt-mTOR pathway and hypoxia-induced factor 1 signaling pathway in gastric cancer cells, resulting in preventative autophagy

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, MCF-7
EMT↓, led to the repression of EMT promotion
E-cadherin↑,
Vim↓,
MMP2↓,
NOTCH1↓, This agent also inhibited Notch1 and PI3K/Akt signalin
PI3K/Akt↓,
PI3k/Akt/mTOR↓,
p‑Akt↓,
EZH2↓, Querectin-3-methyl ether downregulates Notch1, PI3K-AKT and EZH2 signals in breast cancer cells
H3K27ac↓, quercetin-3-methyl ether considerably decreased H3K27 methylation
TumCCA↑, cell cycle dysregulation
CSCs↓, which resulted in the downregulation of protein markers associated with cell cycle, apoptosis, stem cell pluripotency, and self-renewal, including CDK1, Cyclin B1, Bcl-xl, Bcl-2, Sox2 and Nanog
CDK1↓,
CycB/CCNB1↓,
Bcl-xL↓,
Bcl-2↓,
Nanog↓,
H3↓, Treatment with quercetin‑3‑methyl ether alone markedly suppressed the levels of tri‑methyl histone H3 (Lys27)

52- QC,    Effect of Quercetin on Cell Cycle and Cyclin Expression in Ovarian Carcinoma and Osteosarcoma Cell Lines
- in-vitro, BC, MCF-7 - in-vitro, Ovarian, SKOV3 - in-vitro, OS, U2OS
Bcl-2↓, quercetin treatment Bcl-2 expression decreased significantly while Bax expression increased significantly
BAX↑,
PI3K/Akt↓,
cycD1/CCND1↓, The cyclin D1 expression was significantly decreased following the treatment with quercetin in SKOV3 and U2OSPt cells, but not in SKOV3/CDDP and U2OS cells
TumCCA↑, quercetin influenced the G2/M phase of cell cycle, the flavonoid did not affect cyclin B1 levels in all cell lines, indicating the involvement of other possible mechanisms.

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

96- QC,  docx,    Quercetin reverses docetaxel resistance in prostate cancer via androgen receptor and PI3K/Akt signaling pathways
- vitro+vivo, Pca, LNCaP - in-vitro, Pca, PC3
PI3K/Akt↓, PI3K/Akt signaling pathway was excessively activated after prostate cancer cells developed resistance to docetaxel. And quercetin could also reverse the activation of this pathway.
Ki-67↓,
BAX↑,
Bcl-2↓,
EpCAM↓,
Twist↓, Twist2
E-cadherin↑,
P-gp↓, Quercetin reverses docetaxel resistance by reversing the up-regulation of P-gp
TumCP↓, quercetin had the reversal effect of docetaxel-resistance, which could inhibit cell proliferation, migration, invasion and colony formation of docetaxel-resistant prostate cancer cells.
TumCMig↓,
TumCI↓,

99- QC,    Quercetin Inhibits Epithelial-to-Mesenchymal Transition (EMT) Process and Promotes Apoptosis in Prostate Cancer via Downregulating lncRNA MALAT1
- in-vitro, Pca, PC3
EMT↓, quercetin suppressed EMT process, promote apoptosis and deactivated PI3K/Akt signaling pathway in PC-3 cells
E-cadherin↑, Quercetin increased E-cadherin expression and decreased the level of N-cadherin
N-cadherin↓,
Ki-67↓, while the production of Ki67 was significantly reduced by quercetin
PI3K/Akt↓,
MALAT1↓, MALAT1 expression was significantly downregulated in quercetin-treated PC cells at a dose- and time-dependent manne
TumCG↓, Quercetin Inhibited Tumor Growth by Targeting MALAT1 in vivo

82- QC,  ATG,    Arctigenin in combination with quercetin synergistically enhances the anti-proliferative effect in prostate cancer cells
- in-vitro, Pca, LNCaP
AR↓,
PI3K/Akt↓, The combination treatment significantly inhibited both AR and PI3K/Akt pathways compared to control.
miR-21↓,
STAT3↓,
BAD↓,
PRAS40↓,
GSK‐3β↓,
PSA↓,
NKX3.1↑,
Bax:Bcl2↑, a significantly increased ratio of Bax to Bcl-2 protein expression was observed in LAPC-4 cells by the combination treatment compared to Q alone, and a trend to increase in LNCaP cells
miR-19b↓,
miR-148a↓,
AMPKα↓,
TumCP↓, The anti-proliferative activity of arctigenin was 10-20 fold stronger than quercetin in both cell lines.
chemoPv↑, combination of arctigenin and quercetin, that target similar pathways, at low physiological doses, provides a novel regimen with enhanced chemoprevention in prostate cancer.
TumCMig↓, Enhanced inhibition of cell migration

102- RES,    Effect of resveratrol on proliferation and apoptosis of human pancreatic cancer MIA PaCa-2 cells may involve inhibition of the Hedgehog signaling pathway
- in-vitro, PC, MIA PaCa-2
HH↓, the levels of Ihh, Ptch and Smo were decreased by Res treatment
PTCH1↓,
Smo↓,
HH↓, Ihh
EMT↓,
PI3K/Akt↓, thru PI-3K/Akt/NF-κB↓
NF-kB↓,
TumCP↓, Res can inhibit the cell proliferative ability in a time- and dose-dependent manner.
Apoptosis↑, Res further induced apoptosis of MIA PaCa-2 cells in a dose-dependent manner.
ChemoSen↑, The apoptotic rate was significantly increased in cells treated with 5-Fu and Res, and the number of apoptotic cells increased with the increasing concentrations of Res


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:


Redox & Oxidative Stress ⓘ

Catalase↑, 1,   GSH↓, 1,   HK1↓, 1,   HO-1↑, 1,   NRF2↑, 1,   ROS↑, 7,   SOD↑, 2,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 2,   CDC25↓, 1,   MMP↓, 3,   mtDam↑, 1,  

Core Metabolism/Glycolysis ⓘ

ALDOA↓, 1,   AMP↓, 1,   AMPK↑, 1,   ENO1↓, 1,   Glycolysis↓, 1,   HK2↓, 1,   lactateProd↓, 1,   NADPH↓, 1,   PGK1↓, 1,   PI3K/Akt↓, 24,   PI3k/Akt/mTOR↓, 1,   PPP↓, 1,  

Cell Death ⓘ

Akt↓, 3,   p‑Akt↓, 2,   Apoptosis↑, 7,   BAD↓, 2,   BAX↑, 9,   Bax:Bcl2↑, 3,   Bcl-2↓, 9,   Bcl-xL↓, 2,   BID↑, 1,   Casp↑, 2,   Casp3↑, 5,   Casp8↑, 1,   Casp9↑, 6,   CK2↓, 1,   Cyt‑c↑, 3,   hTERT/TERT↓, 1,   iNOS↓, 1,   MAPK↓, 1,   MAPK↑, 1,   MAPK↝, 1,   Mcl-1↓, 1,   p27↑, 2,   survivin↓, 2,  

Kinase & Signal Transduction ⓘ

AMPKα↓, 1,   HER2/EBBR2↓, 2,   RTK-RAS↓, 1,  

Transcription & Epigenetics ⓘ

EZH2↓, 1,   H3↓, 1,   HATs↓, 1,   miR-21↓, 1,  

Protein Folding & ER Stress ⓘ

HSP90↓, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,   NKX3.1↑, 1,   P53↑, 3,   PARP↑, 2,   cl‑PARP↑, 1,  

Cell Cycle & Senescence ⓘ

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

Proliferation, Differentiation & Cell State ⓘ

cMET↓, 1,   CSCs↓, 2,   EMT↓, 4,   EpCAM↓, 1,   ERK↓, 4,   ERK↑, 1,   FOXO↓, 1,   Gli1↓, 1,   GSK‐3β↓, 1,   H3K27ac↓, 1,   HH↓, 3,   IGF-1↓, 1,   Let-7↑, 1,   mTOR↓, 4,   p‑mTOR↓, 1,   Nanog↓, 1,   NOTCH1↓, 3,   P70S6K↓, 1,   PTCH1↓, 2,   PTEN↑, 1,   Smo↓, 1,   Src↓, 1,   STAT↓, 1,   p‑STAT↓, 1,   STAT3↓, 4,   Sufu↓, 1,   TumCG↓, 4,   Wnt/(β-catenin)↓, 2,  

Migration ⓘ

E-cadherin↑, 4,   p‑FAK↓, 1,   Ki-67↓, 2,   MALAT1↓, 1,   miR-148a↓, 1,   miR-19b↓, 1,   MMP2↓, 4,   MMP7↓, 1,   MMP9↓, 4,   N-cadherin↓, 1,   TGF-β↓, 1,   TIMP1↑, 1,   TIMP2↑, 1,   TumCI↓, 4,   TumCMig↓, 5,   TumCP↓, 6,   Twist↓, 1,   Vim↓, 2,   Zeb1↓, 1,   ZEB2↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   EGFR↓, 4,   HIF-1↓, 3,   Hif1a↓, 3,   VEGF↓, 4,  

Barriers & Transport ⓘ

GLUT1↓, 3,   GLUT4↓, 1,   P-gp↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 3,   IFN-γ↓, 1,   IKKα↓, 2,   IL6↓, 2,   IL8↓, 1,   JAK↓, 1,   p‑JAK↓, 1,   NF-kB↓, 8,   PSA↓, 1,   TNF-α↓, 1,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 4,   eff↓, 1,   eff↑, 1,   selectivity↑, 1,  

Clinical Biomarkers ⓘ

AR↓, 1,   E6↓, 1,   E7↓, 1,   EGFR↓, 4,   EZH2↓, 1,   HER2/EBBR2↓, 2,   hTERT/TERT↓, 1,   IL6↓, 2,   Ki-67↓, 2,   PSA↓, 1,  

Functional Outcomes ⓘ

chemoPv↑, 2,   PRAS40↓, 1,   toxicity↓, 1,  
Total Targets: 150

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

Catalase↑, 1,   GPx↑, 1,   HO-1↑, 1,   Keap1↓, 1,   NRF2↑, 1,  

Functional Outcomes ⓘ

toxicity↑, 1,  
Total Targets: 6

Scientific Paper Hit Count for: PI3K/Akt, PI3K/Akt signaling
9 Quercetin
3 Apigenin (mainly Parsley)
3 EGCG (Epigallocatechin Gallate)
3 Garcinol
2 Cisplatin
2 Arctigenin
2 Curcumin
2 Docetaxel
2 Deguelin
1 Allicin (mainly Garlic)
1 Paclitaxel
1 Graviola
1 doxorubicin
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#:%  Target#:253  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

 

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