Leptin induces cell proliferation and reduces cell apoptosis by activating c-myc in cervical cancer

Abstract

Leptin may be involved in the pathogenesis of numerous cancer types by activation of cellular signal-transduction pathways. In this study, we analyzed the role of leptin and the mechanism(s) underlying its action in cervical carcinoma cells. Firstly, we examined the expression of leptin in 80 cases of cervical carcinoma using immunohistochemical staining. The results showed that the levels of leptin correlated significantly with the grades of cervical carcinoma. At the same time, the expression of leptin correlated positively with c-myc and its downstream gene, bcl-2. The expression of c-myc and bcl-2 was evaluated in leptin-treated HeLa cells by reverse transcription-polymerase chain reaction (RT-PCR) and western blotting. Recombinant leptin significantly activated the expression of bcl-2 and c-myc in HeLa cells. Finally, the apoptotic index, the proliferative activity and the expression levels of c-myc and bcl-2 were determined in the HeLa cells treated with silencing of leptin. We found that silencing of leptin inhibited the proliferation of HeLa cells and reduced the expression of bcl-2 and c-myc. Our data demonstrated that leptin interferes with the expression of oncogenic c-myc and anti-apoptotic bcl-2, and regulates cell turnover and facilitates the progression of cervical cancer.