Erratum: CRIPTO overexpression promotes mesenchymal differentiation in prostate carcinoma cells through parallel regulation of AKT and FGFR activities.
Because the major reason for the limited efficacy of PI3K/Akt-targeted therapies in prostate cancer (PCa) is loss of mTOR-regulated feedback suppression, it is therefore important to assess the functional importance and regulation of GRB10 under these conditions.
Importantly, silence of PP1α reversed the inhibitory effect of MIIP on AKT phosphorylation and cell growth in PCa cell lines, while MIIP∆C, which is incapable of interacting with PP1α, loses MIIP's effect, suggesting that MIIP exerts its roles via interaction with PP1α.
Ectopic overexpression of FGFR3-S in European American (EA) prostate cancer cell lines (PC-3 and LNCaP) led to enhanced receptor autophosphorylation and increased activation of the downstream signaling effectors AKT, STAT3, and ribosomal S6 compared with FGFR3-L (retains exon 14).
Our study demonstrates the potential clinical utility of PTEN genomic deletion in low-intermediate risk patients and highlights the enhanced prognostication achieved when assessed in combination with another genomic biomarker related to the PI3K/AKT pathway, thereby supporting their promising usefulness in clinical management of prostate cancer.
We show <i>Pik3ca</i><sup>H1047R</sup> mutation causes p110α-dependent invasive prostate carcinoma <i>in vivo</i> Furthermore, we report that <i>PIK3CA</i> mutation and <i>PTEN</i> loss coexist in patients with prostate cancer and can cooperate <i>in vivo</i> to accelerate disease progression via AKT-mTORC1/2 hyperactivation.
Preclinical characterization of <b>10h</b>, a promising lead AKT inhibitor, as a potential anti-prostate cancer therapeutic needs to be further investigated.