SHIP2 inhibition alters redox-induced PI3K/AKT and MAP kinase pathways via PTEN over-activation in cervical cancer cells.

ABSTRACT: Phosphatidylinositol (3,4,5)-trisphosphate (PI(3,4,5)P3) is required for protein kinase B (AKT) activation. The level of PI(3,4,5)P3 is constantly regulated through balanced synthesis by phosphoinositide 3-kinase (PI3K) and degradation by phosphoinositide phosphatases phosphatase and tensin homologue (PTEN) and SH2-domain containing phosphatidylinositol-3,4,5-trisphosphate 5-phosphatase 2 (SHIP2), known as negative regulators of AKT. Here, I show that SHIP2 inhibition in cervical cancer cell lines alters H₂ O₂ -mediated AKT and mitogen-activated protein kinase/extracellular signal-regulated kinase pathway activation. In addition, SHIP2 inhibition enhances reactive oxygen species generation. Interestingly, I found that SHIP2 inhibition and H₂ O₂ t

SUBMITTER: Azzi A 

PROVIDER: S-EPMC7530381 | biostudies-literature | 2020 Oct

REPOSITORIES: biostudies-literature