Cervical cancer is the second most common and malignant tumor among women worldwide. However, the effective therapies for this deadly disease are limited because the elaborate molecular mechanism of progress of cervical cancer remains largely unknown. In present study, we not only determine the miR-182 as an anticancer miRNA molecule but also provide the mechanistic link between miR-182 and its anticancer activity. Primarily, the expression of miR-182 is significantly down-regulated in cervical tumor in contrast to normal cervical tissue, and then miR-182 mimic-treated cell presents reduction of cell proliferation and promoting apoptosis. During this process, DNA methyltransferase 3a (DNMT3a) expression is markedly decreased, thereby likely contributing to miR-182-induced apoptosis. Consistently, over-expression of DNMT3a inhibits the miR-182-induced apoptosis, and inhibition of DNMT3a promotes cervical cancer cell apoptosis, which further demonstrated that DNMT3a involved in cervix carcinogenesis. Collectively, we have revealed a valuable mechanism by which down-regulation of DNMT3a contributes to the miR-182-induced cervical cancer cell apoptosis, which raise a becoming potential that miR-182 administration or inhibition of DNMT3a expression may be the underlying strategies for therapeutic intervention in cervical carcinoma.
Keywords: Cervical cancer; DNMT3a; apoptosis; miR-182.