PI3k/Akt/mTOR Cancer Research Results

PI3k/Akt/mTOR, Phosphoinositide 3-kinase/Protein Kinase B/ mammalian target of rapamycin: Click to Expand ⟱
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The PI3K/Akt/mTOR signaling pathway is a critical regulator of cell growth, proliferation, survival, and metabolism.

In many cancers (such as breast, colorectal, lung, and endometrial cancers), the PI3K/Akt/mTOR pathway is often hyperactivated.

– This hyperactivation is frequently due to gene mutations (e.g., in PIK3CA), loss of PTEN, and amplification events that enhance the pathway’s activity.

– Increased activity is also observed via elevated levels of phosphorylated Akt and mTOR in tumors compared to normal tissues.
Scientific Papers found: Click to Expand⟱
242- Api,    Apigenin inhibits proliferation and invasion, and induces apoptosis and cell cycle arrest in human melanoma cells
- in-vitro, Melanoma, A375 - in-vitro, Melanoma, C8161
ERK↓,
PI3k/Akt/mTOR↓, Akt/mTOR
Casp3↑, cleaved
PARP↑, cleaved
p‑mTOR↓,
p‑Akt↓,

124- CUR,    Curcumin-Gene Expression Response in Hormone Dependent and Independent Metastatic Prostate Cancer Cells
- in-vitro, Pca, LNCaP - in-vitro, Pca, C4-2B
TGF-β↓, significantly regulated top canonical pathways highlighted that Transforming growth factor beta (TGF-β), Wingless-related integration site (Wnt), Phosphoinositide 3-kinase/Protein Kinase B/ mammalian target of rapamycin (PIK3/AKT(PKB)/mTOR)
Wnt↓,
PI3k/Akt/mTOR↓,
NF-kB↓, and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) signaling were primarily inhibited
PTEN↑,
Apoptosis↑,
TumCCA↑, Phosphatase and tensin homolog (PTEN) dependent cell cycle arrest and apoptosis pathways were elevated with curcumin treatment.

468- CUR,  5-FU,    Gut microbiota enhances the chemosensitivity of hepatocellular carcinoma to 5-fluorouracil in vivo by increasing curcumin bioavailability
- vitro+vivo, Liver, HepG2 - vitro+vivo, Liver, 402 - vitro+vivo, Liver, Bel7
Apoptosis↑,
TumCCA↑, G2/M cell cycle arrest
PI3k/Akt/mTOR↓,
p‑PI3K↓,
Bacteria↑, gut microbiota: Lactobacillus, Epsilonbacteraeota, Helicobacterac-eae, Campylobacterales, Helicobacter, Escherichia-shigella, Bifidobacterium, Campylobacteria
cl‑Casp3↑,

452- CUR,    Curcumin downregulates the PI3K-AKT-mTOR pathway and inhibits growth and progression in head and neck cancer cells
- vitro+vivo, HNSCC, SCC9 - vitro+vivo, HNSCC, FaDu - vitro+vivo, HNSCC, HaCaT
TumCCA↑, arrested cell cycle at phase G2 /M
PI3k/Akt/mTOR↓,
Casp3↑,
EGFR↓, 0.18 fold
EGF↑, Curcumin induced a noticeable increase in the expression of EGF (11.3-fold change)
PRKCG↑, 13.2 fold
p‑Akt↓,
p‑mTOR↓,
RPS6KA1↓, 0.17 fold
EIF4E↓, 0.18 fold
proCasp3↓,

676- EGCG,  Chemo,    The Potential of Epigallocatechin Gallate (EGCG) in Targeting Autophagy for Cancer Treatment: A Narrative Review
- Review, NA, NA
PI3k/Akt/mTOR↓,
Apoptosis↑,
ROS↑,
TumAuto↑,

948- F,    Low Molecular Weight Fucoidan Inhibits Tumor Angiogenesis through Downregulation of HIF-1/VEGF Signaling under Hypoxia
- vitro+vivo, Bladder, T24/HTB-9 - in-vitro, Nor, HUVECs
p‑PI3k/Akt/mTOR↓,
p‑p70S6↓,
p‑4E-BP1↓,
angioG↓, did not affect angiogenesis under normoxic conditions (data not shown), suggesting the antiangiogenic activity of LMWF is hypoxia specific.
Hif1a↓,
VEGF↑,
TumCG↓,
TumVol↓, in mice (needed 300mg/kg/day to actually shrink tumor as opposed to slowing growth)
TumW↓, in mice
Iron∅, maintaining Fe2+ availability through suppression of hypoxia-induced ROS formation is crucial for promoting HIF-1 degradation and diminishing HIF-1 activity by preventing PHD and FIH inactivation
ROS↓, LMWF may target different levels, including inhibition of ROS formation

62- QC,  GoldNP,    Gold nanoparticles-conjugated quercetin induces apoptosis via inhibition of EGFR/PI3K/Akt-mediated pathway in breast cancer cell lines (MCF-7 and MDA-MB-231)
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231
EGFR↓, AuNPs-Qu-5 treatment inhibited the EGFR and its downstream signalling molecules PI3K/Akt/mTOR/GSK-3β.
PI3k/Akt/mTOR↓, PI3K/Akt/mTOR/GSK-3β
GSK‐3β↓,
TumCP↓, AuNPs-Qu-5 in breast cancer cell lines curtails cell proliferation through induction of apoptosis and also suppresses EGFR signalling.
Apoptosis↑,
tumCV↓, Cell viability of free AuNPs, free Qu, and AuNPs‐Qu‐5 was tested on breast cancer cell lines (MCF‐7 and MDA‐MB‐231), and it was found that free Qu and AuNPs‐Qu‐5 decreased the cell viability.
mTOR↓, AuNPs‐Qu‐5 treated cells downregulated mTOR protein and upregulated PTEN protein expression compared to free Qu
PTEN↑,

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)

910- QC,    The Anti-Cancer Effect of Quercetin: Molecular Implications in Cancer Metabolism
tumCV↓,
Apoptosis↑,
PI3k/Akt/mTOR↓, QUE induces cell death by inhibiting PI3K/Akt/mTOR and STAT3 pathways in PEL cells
Wnt/(β-catenin)↓, reducing β-catenin
MAPK↝,
ERK↝, ERK1/2
TumCCA↑, cell cycle arrest at the G1 phase
H2O2↑,
ROS↑,
TumAuto↑,
MMPs↓, Consistently, QUE was able to reduce the protein levels of MMP-2, MMP-9, VEGF and mTOR, and p-Akt in breast cancer cell lines
P53↑,
Casp3↑,
Hif1a↓, by inactivating the Akt-mTOR pathway [64,74] and HIF-1α
cFLIP↓,
IL6↓, QUE decreased the release of interleukin-6 (IL-6) and IL-10
IL10↓,
lactateProd↓,
Glycolysis↓, It is suggested that QUE alters glucose metabolism by inhibiting monocarboxylate transporter (MCT) activity
PKM2↓,
GLUT1↓,
COX2↓,
VEGF↓,
OCR↓,
ECAR↓,
STAT3↓,
MMP2↓, Consistently, QUE was able to reduce the protein levels of MMP-2, MMP-9, VEGF and mTOR, and p-Akt in breast cancer cell lines
MMP9:TIMP1↓,
mTOR↓,

1208- SANG,    Sanguinarine induces apoptosis in osteosarcoma by attenuating the binding of STAT3 to the single-stranded DNA-binding protein 1 (SSBP1) promoter region
- in-vitro, OS, NA
SSBP1↑,
mtDam↑,
Apoptosis↑,
JAK↓,
STAT3↓,
PI3k/Akt/mTOR↓,
ROS↑,
MMP↓,

962- TQ,    Thymoquinone affects hypoxia-inducible factor-1α expression in pancreatic cancer cells via HSP90 and PI3K/AKT/mTOR pathways
- in-vitro, PC, PANC1 - in-vitro, Nor, hTERT-HPNE - in-vitro, PC, AsPC-1 - in-vitro, PC, Bxpc-3
TumCMig↓,
TumCI↓,
Apoptosis↑, no significant effects on hTERT-HPNE cells (normal cells) ****
Hif1a↓, TQ significantly reduced the mRNA and protein expression levels of HIF-1α in PANC-1, AsPC-1, and BxPC-3 cells.
PI3k/Akt/mTOR↓,
TumCCA↑, possible mechanism of TQ's influence on PC cell cycle was that TQ inhibited the proliferation of cancer cells (reducing the proportion of S phase) and damaged the DNA of cancer cells (increasing the proportion of G2/M phase). No effect on normal cell
*toxicity↓, TQ had no significant effect on the viability of hTERT-HPNE cells
*TumCI∅, no significant difference in the invasion ability of the hTERT-HPNE cells
*TumCMig∅, no significant effect on the migration and invasion of normal pancreatic ductal epithelial cells.


Showing Research Papers: 1 to 11 of 11

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 11

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

H2O2↑, 1,   Iron∅, 1,   ROS↓, 1,   ROS↑, 3,  

Mitochondria & Bioenergetics ⓘ

EGF↑, 1,   MMP↓, 1,   mtDam↑, 1,   OCR↓, 1,   SSBP1↑, 1,  

Core Metabolism/Glycolysis ⓘ

ECAR↓, 1,   Glycolysis↓, 1,   lactateProd↓, 1,   PI3K/Akt↓, 1,   PI3k/Akt/mTOR↓, 10,   p‑PI3k/Akt/mTOR↓, 1,   PKM2↓, 1,  

Cell Death ⓘ

p‑Akt↓, 3,   Apoptosis↑, 7,   Bcl-2↓, 1,   Bcl-xL↓, 1,   Casp3↑, 3,   cl‑Casp3↑, 1,   proCasp3↓, 1,   cFLIP↓, 1,   MAPK↝, 1,  

Kinase & Signal Transduction ⓘ

p‑p70S6↓, 1,  

Transcription & Epigenetics ⓘ

EZH2↓, 1,   H3↓, 1,   tumCV↓, 2,  

Autophagy & Lysosomes ⓘ

TumAuto↑, 2,  

DNA Damage & Repair ⓘ

P53↑, 1,   PARP↑, 1,  

Cell Cycle & Senescence ⓘ

CDK1↓, 1,   CycB/CCNB1↓, 1,   TumCCA↑, 6,  

Proliferation, Differentiation & Cell State ⓘ

p‑4E-BP1↓, 1,   CSCs↓, 1,   EIF4E↓, 1,   EMT↓, 1,   ERK↓, 1,   ERK↝, 1,   GSK‐3β↓, 1,   H3K27ac↓, 1,   mTOR↓, 2,   p‑mTOR↓, 2,   Nanog↓, 1,   NOTCH1↓, 1,   p‑PI3K↓, 1,   PRKCG↑, 1,   PTEN↑, 2,   RPS6KA1↓, 1,   STAT3↓, 2,   TumCG↓, 1,   Wnt↓, 1,   Wnt/(β-catenin)↓, 1,  

Migration ⓘ

E-cadherin↑, 1,   MMP2↓, 2,   MMP9:TIMP1↓, 1,   MMPs↓, 1,   TGF-β↓, 1,   TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 1,   Vim↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   EGFR↓, 2,   Hif1a↓, 3,   VEGF↓, 1,   VEGF↑, 1,  

Barriers & Transport ⓘ

GLUT1↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   IL10↓, 1,   IL6↓, 1,   JAK↓, 1,   NF-kB↓, 1,  

Clinical Biomarkers ⓘ

EGFR↓, 2,   EZH2↓, 1,   IL6↓, 1,  

Functional Outcomes ⓘ

TumVol↓, 1,   TumW↓, 1,  

Infection & Microbiome ⓘ

Bacteria↑, 1,  
Total Targets: 81

Pathway results for Effect on Normal Cells:


Migration ⓘ

TumCI∅, 1,   TumCMig∅, 1,  

Functional Outcomes ⓘ

toxicity↓, 1,  
Total Targets: 3

Scientific Paper Hit Count for: PI3k/Akt/mTOR, Phosphoinositide 3-kinase/Protein Kinase B/ mammalian target of rapamycin
3 Curcumin
3 Quercetin
1 Apigenin (mainly Parsley)
1 5-fluorouracil
1 EGCG (Epigallocatechin Gallate)
1 Chemotherapy
1 Fucoidan
1 Gold NanoParticles
1 Sanguinarine
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

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