Activation of phosphatidylinositol 3-kinase-protein kinase B(PI3K-PKB) induced by 17?-estradiol in endometrial carcinoma cell (Ishikawa) / 中华妇产科杂志

ABSTRACT

Objective Cellular response to estradiol is mediated both by estrogen receptor (ER) binding to estrogen response element (ERE) and by non-nuclear actions like activation of signal transduction pathways such as mitogen activated protein kinase (MAPK) pathway. However, the signal transduction of estrogen involving phosphatidylinositol 3-kinase-protein kinase B (PI3K -PKB) is not clear in endometrial carcinoma. Our purpose was to study if PI3K-PKB signaling pathway could be activated rapidly by 17?-E 2 through non-nuclear action and also, whether PI3K inhibitor, LY294002, could inhibit such non-nuclear action of 17?-E 2 in endometrial carcinoma cell line Ishikawa. Methods Levels of phosphorylated PKB(Ser473 site, p-PKB) and total PKB were examined by western blotting in Ishikawa cells after stimulation with 17?-E 2 at 1?10 -6 mol/L for different time periods and at varied doses for 30 min. Optimal time and appropriate dose for 17?-E 2 to activate PKB in Ishikawa cells were observed. Inhibitory effect of LY294002 on activation of PKB induced by 17?-E 2 was also studied. p-PKB/PKB ratio was used to indicate levels of activation of PKB. Results p-PKB/PKB at 15 min (0.533?0.029) was significantly higher than the control (0.361?0.029, P 0.05, 0.05,