Signaling mechanisms coupled to CXCL12/CXCR4-mediated cellular proliferation are PTEN-dependent.

摘要: A key difference between normal and malignant prostate cells in vitro vivo is that both alleles of PTEN are largely intact benign glands cultured epithelial cells, whereas one or mutant deleted the majority tumors cancer cell lines. Intact suppresses phosphorylation Akt downstream PI3K activation non-transformed unimpeded often PTEN-deficient. We have previously shown CXCL12/CXCR4 axis transactivates EGFR to promote pro-proliferative signaling preferentially through Raf/MEK/Erk pathway cells. These demonstrate little basal pAkt these levels do not increase with CXCL12 stimulation because fully functional. Thus, inactivation may be critical factor modulates specific CXCL12-stimulated proliferative responses transformed Based on data, we hypothesize CXCL12/CXCR4-mediated PI3K/Akt pathways modulated by status.