The Role Of ERK1/2 In Leptin Promoting The Proliferation Of Human Endometrial Cancer Cells

Objective To investigate the role of ERK1/2 in leptin promoting the proliferation of human endometrial cancer cells.Methods The expression of leptin receptor (OB-Rb) in Ishikawa cells was detected by fluoroimmunoassay. The cells were treated by leptin with various concentrations (0ng/ml, 10ng/ml, 50ng/ml, 100ng/ml, 150ng/ml) for different time (6h, 12h, 24h). The effect of leptin on cell proliferation was examined by MTT assay. Meanwhile, inhibitory effect of ERK1/2 selective inhibitor PD98059, which blocks ERK1/2 phosphorylation, on the proliferation of Ishikawa cells induced by leptin was also studied. Ishikawa cells were treated with 100ng/ml leptin for various time periods (20min, 40min, 60min), then the level of phosphorylated ERK1/2 (p-ERK1/2) and ERK1/2 were examined by Western Blot. Results Fluoroimmunoassay showed the presence of OB-Rb in Ishikawa cells.Leptin (0ng/ml～100ng/ml) stimulated the proliferation of Ishikawa cells in a dose-dependent manner. This effect was maximum at 100ng/ml for 24h treatment, and there was no difference between 100ng/ml and 150ng/ml group. Blocking ERK1/2 phosphorylation by PD98059 significantly reduced the proliferation of Ishikawa cells stimulated by leptin in a dose-dependent manner. Western Blot showed that ERK1/2 phosphorylation increased significantly stimulated by leptin in Ishikawa cells, and lasted for 60min at least.Conclusion It is suggested that leptin may promote the proliferation of endometrial cancer cells by activating ERK1/2 signaling pathway.