Application | Comment | Organism |
---|---|---|
medicine | prolyl carboxypeptidase and prolyl endopeptidase regulate insulin receptor substrate IRS-1 stability and PI3K/AKT activation in pancreatic cancer | Homo sapiens |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Homo sapiens | - |
- |
- |
Source Tissue | Comment | Organism | Textmining |
---|---|---|---|
CAPAN-1 cell | pancreatic cancer cell line | Homo sapiens | - |
PANC-1 cell | pancreatic cancer cell line | Homo sapiens | - |
PK-9 cell | pancreatic cancer cell line | Homo sapiens | - |
General Information | Comment | Organism |
---|---|---|
physiological function | prolyl carboxypeptidase and the related family member prolyl endopeptidase are essential for proliferation and survival of pancreatic cancer cells. Depletion/inhibition of prolyl carboxypeptidase and prolyl endopeptidase induces serine phosphorylation and degradation of insulin receptor substrate IRS-1, leading to inactivation of the cellular PI3K and AKT. Depletion/inhibition of prolyl carboxypeptidase /prolyl endopeptidase destabilized IRS-1 in the cells treated with rapamycin, blocking the feedback activation PI3K/AKT. Inhibition of prolyl carboxypeptidase /prolyl endopeptidase enhances rapamycin-induced cytotoxicity | Homo sapiens |