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Objective: To investigate leptin JAK2/STAT3 signal transduction pathway in promoting proliferation of endometrial cancer in rats. Methods: Immunofluorescence Ishikawa cells leptin receptor (OB-Rb) expression . Ishikawa cells were added at different concentrations of leptin (0,10,50,100,150 ng / ml), the role of different time (6,12,24 h), MTT assay cell proliferation in each group ; same law apply different concentration (10,50,100 μmol / L) JAK2 kinase inhibitor AG490 blocked STAT3 phosphorylation, leptin stimulated Ishikawa cell proliferation ; using immunoblotting (Western blot) leptin (100ng/ml) role Ishikawa cells at different times (0,20,40,60 min) its phosphorylation of STAT3 . Results: Immunofluorescence Ishikawa cells confirmed the presence of leptin receptor (OB-Rb) expression ; leptin can significantly promote the proliferation of Ishikawa cells in a time and dose-dependent manner , while at 100ng/ml for 24h proliferative effect of leptin maximum , 100ng/ml and 150ng/ml group there was no significant difference (P gt; 0.05); AG490 can inhibit the proliferation of leptin on Ishikawa cells with AG490 concentration, inhibition gradually increased ; Ishikawa cells were treated with 100ng/ml leptin treatment, with time gradually increased activation of STAT3 , and continued for at least 60min. Conclusions: Leptin may activate JAK2/STAT3 signal transduction pathway promotes the proliferation of endometrial cancer .
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