Effect of Leptin on the Proliferation and Apoptosis of Ovarian Carcinoma SKOV3 Cells
Xi Jiang
Abstract
Xi Jiang
Abstract
Objective: To investigate the effect and the underlying molecular mechanism of leptin on the proliferation and apoptosis of ovarian carcinoma SKOV3 cells. Methods: After stimulation with various doses of leptin(0, 50, 100, 200 ng/m L) for 48 h,the cell proliferation rate was analyzed by MTT colorimetry. Serum deprivation was used to induce cell apoptosis in SKOV3 cells stimulated with leptin. Cell apoptosis was assessed by double staining with Annexin V and propidium iodide. The expression levels of p21, cyclin D1, Bcl-2, Bax and ERK1/2 pathway were detected by western blotting. Results: Leptin promoted the cell proliferation and dampened the apoptosis rates induced by serum deprivation in a dose-dependent manner. Furthermore, leptin treatment down-regulated the expression levels of p21, up-regulated the cyclin D1 expression. Moreover, an obvious down-regulation of Bax protein and up-regulation of Bcl-2 was confirmed in SKOV3 cell treated with leptin. Leptin dramatically induced the activation of ERK1/2 pathway,and blocking this pathway with its inhibitor PD98059 strikingly attenuated leptin-induced proliferation and anti-apoptosis effect in SKOV3 cell, concomitant with the decrease of cyclin D1 and Bcl-2 expression and increase of Bax expression. Conclusion: Leptin could promote the SKOV3 cell proliferation and inhibit the apoptosis by the activation of ERK1/2 signaling to regulate SKOV3 cell mitosis and expression levels of apoptosis-related protein.
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Objective: To investigate the effect and the underlying molecular mechanism of leptin on the proliferation and apoptosis of ovarian carcinoma SKOV3 cells. Methods: After stimulation with various doses of leptin(0, 50, 100, 200 ng/m L) for 48 h,the cell proliferation rate was analyzed by MTT colorimetry. Serum deprivation was used to induce cell apoptosis in SKOV3 cells stimulated with leptin. Cell apoptosis was assessed by double staining with Annexin V and propidium iodide. The expression levels of p21, cyclin D1, Bcl-2, Bax and ERK1/2 pathway were detected by western blotting. Results: Leptin promoted the cell proliferation and dampened the apoptosis rates induced by serum deprivation in a dose-dependent manner. Furthermore, leptin treatment down-regulated the expression levels of p21, up-regulated the cyclin D1 expression. Moreover, an obvious down-regulation of Bax protein and up-regulation of Bcl-2 was confirmed in SKOV3 cell treated with leptin. Leptin dramatically induced the activation of ERK1/2 pathway,and blocking this pathway with its inhibitor PD98059 strikingly attenuated leptin-induced proliferation and anti-apoptosis effect in SKOV3 cell, concomitant with the decrease of cyclin D1 and Bcl-2 expression and increase of Bax expression. Conclusion: Leptin could promote the SKOV3 cell proliferation and inhibit the apoptosis by the activation of ERK1/2 signaling to regulate SKOV3 cell mitosis and expression levels of apoptosis-related protein.
Key concepts: Apoptosis, Leptin, Propidium iodide, Cell growth, Cyclin D1, Annexin, Cell cycle, Cyclin B1