mTORC2 Cancer Research Results

mTORC2, mammalian target of rapamycin (mTOR) complex 2: Click to Expand ⟱
Source:
Type:
mTORC2 associates closely with the plasma membrane, and has been detected in association with ribosomal membranes (11), where it can interact with its key substrates, the AGC kinases including AKT1-3, serum glucose kinase (SGK) isoforms, and protein kinase C (PKC) family members.
Rapamycin is a known allosteric inhibitor of mTORC1, while TOR kinase inhibitors (TOR-KIs) inhibit the activities of both complexes.
AKT, a key substrate of mTORC2, is among the most commonly hyper-activated proteins in cancer. AKT integrates signals from PI3K/mTORC2 and from PI3K/PDK1 to promote cell growth and survival.
Scientific Papers found: Click to Expand⟱
6547- BSB,    Antitumor effects of a-bisabolol against pancreatic cancer
- vitro+vivo, PC, PANC1 - in-vitro, PC, MIA PaCa-2 - in-vitro, PC, KLM1 - in-vitro, PC, KP4 - in-vitro, Nor, ACBRI515
TumCP↓, Bisabolol induced a decrease in cell proliferation and viability in pancreatic cancer cell lines (KLM1, KP4, Panc1, MIA Paca2), but not in pancreatic epithelial cells (ACBRI515).
selectivity↑,
Apoptosis↑, α-Bisabolol treatment induced apoptosis and suppressed Akt activation in pancreatic cancer cell lines.
Akt↓,
EGR1↑, α-bisabolol treatment induced the overexpression of early growth response-1 (EGR1), whereas EGR1 siRNA decreased the α-bisabolol-induced cell death of KLM1 cells.
TumCG↓, Tumor growth in both subcutaneous and peritoneal xenograft nude mouse models was significantly inhibited by intragastric administration of 1000 mg/kg of α-bisabolol, once a week for three weeks.
Dose↝, intragastric administration 1000 mg/kg of α-bisabolol, once a week for three weeks.
PI3K↓, in the present study, we found that a-bisabolol inhibited Akt activation, as well as the expression of its upstream signals (PI3K, PDK1, and mTORC2).
PDK1↓,
mTORC2↑,

2847- FIS,    Fisetin-induced cell death, apoptosis, and antimigratory effects in cholangiocarcinoma cells
- in-vitro, CCA, NA
tumCV↓, Fisetin was significant in suppressing CCA cell viability and colony formation during the course of this experiment.
ChemoSen↑, fisetin significantly potentiated the cisplatin-induced CCA cells death
TumCMig↓, reduced the migration of cancer cells and demonstrated more pronounced effects on KKU-M452 cells
ROS↑, fisetin prompted cell death and apoptosis in CCA cells by stimulating the generation of ROS in KKU-100 cells at a dosage of 50 μM
TumCI↓, suppression of cell invasion and migration,prevention of angiogenesis
angioG↓,
CDK2↓, mechanisms including the suppression of cyclin-dependent kinases, the inhibition of PI3K/Akt/mTOR
PI3K↓,
Akt↓,
mTOR↓,
EGFR↓, suppression of the EGFR pathway, the stimulation of the caspase cascade
Casp↑,
mTORC1↓, suppressing the mTORC1 and 2 signaling
mTORC2↑,
cycD1/CCND1↓, decreasing the level of the cyclin D1 and cyclin E mRNA
cycE/CCNE↓,
MMP2↓, Matrix metalloproteinases (MMP) 2 and MMP 9 gene expression and enzyme activity are suppressed
MMP9↓,
ER Stress↑, Moreover, fisetin also caused endoplasmic reticulum (ER) stress-induced production of mitochondrial ROS generation and Ca2+, with the involvement of MAPK signaling
Ca+2↑,
eff↓, The ROS scavenger molecule N-acetyl cysteine decreased fisetin-activated apoptosis in multiple myeloma and oral cancer cells


Showing Research Papers: 1 to 2 of 2

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

ROS↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

PDK1↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 2,   Apoptosis↑, 1,   Casp↑, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

tumCV↓, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

ER Stress↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK2↓, 1,   cycD1/CCND1↓, 1,   cycE/CCNE↓, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

mTOR↓, 1,   mTORC1↓, 1,   mTORC2↑, 2,   PI3K↓, 2,   TumCG↓, 1,  

Migration(tgid=13) ⓘ

Ca+2↑, 1,   MMP2↓, 1,   MMP9↓, 1,   TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 1,   EGFR↓, 1,   EGR1↑, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

ChemoSen↑, 1,   Dose↝, 1,   eff↓, 1,   selectivity↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

EGFR↓, 1,  
Total Targets: 29

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: mTORC2, mammalian target of rapamycin (mTOR) complex 2
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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