"By opposing PI3K signaling, PTEN inhibits the activation of the critical PI3K effector proteins Akt1-3 (also known as protein kinase B or PKB)."
"Exposure of eol-1r cells to imatinib failed to dephosphorylate akt, erk and stat5, although pdgfralpha was effectively inactivated. The forced expression of pten negatively regulated these signal pathways and sensitized eol-1r cells to imatinib."
"On the other hand, AKT1 is negatively regulated by PTEN, a p53 response gene that is inactivated in a variety of cancers XREF_BIBR."
"Phosphatase and tensin homolog (PTEN) negatively regulates downstream protein kinase B signaling, resulting in decreased cellular growth and proliferation."
"Whereas PTEN and Delta85 both inhibited activation of AKT and protein kinase B, only Deltap85 inhibited c-Jun NH2-terminal kinase (JNK) activity."
"Furthermore, overexpression of miR-494-3p inhibited PTEN expression and consequently activated the downstream phosphoinositide3-kinase and protein kinaseB (PI3K and AKT) signialing pathway."
"Recent studies have shown that a loss of PTEN causes continuous activation of protein kinase B (Akt), which is critical in the phosphoinositide 3-kinase (PI3K)-Akt pathway that leads to cell proliferation.9, 10, 11 When NSCLC with low PTEN expression is treated with TKIs, resistance will occur.12 Therefore, TKI resistance could be reversed by upregulating PTEN expression levels."
"Result also showed that CTN could increase expression levels of PTEN, and reduce the phosphorylated levels of Akt (protein kinase B) on Thr 308 and Ser 473 domain."
"In recent studies, there has been consensus that a high percentage of PTEN loss and presence of p-Akt1 in TNBC indicates poor disease-free survival [XREF_BIBR]."
"PTEN is a natural inhibitor of AKT1, an oncogenic kinase that acts downstream of PI3K to control proliferation and survival."