MiR-27b is upregulated in cervical carcinogenesis and promotes cell growth and invasion by regulating CDH11 and epithelial-mesenchymal transition.

Abstract

Dysregulation of microRNAs (miRNAs) occurs frequently in cervical carcinogenesis. miRNAs function as tumor-suppressors or oncogenes and are involved in tumor behavior. However, the expression and function of miR-27b in cervical carcinogenesis remain unknown. In the present study, we observed that miR-27b was significantly increased in cervical cancer cells and tissues, and upregulation of miR-27b was negatively associated with its direct target, cadherin11 (CDH11). Upregulation of miR-27b significantly accelerated the proliferation, cell cycle transition fromG1 to Sphase, migration and invasion of C33A cells, while downregulation of miR-27b suppressed the proliferation and invasion of HeLa cells. Moreover, CDH11 cDNA transfection impaired the oncogenic effect of miR-27b on cancer cells. Knockdown of CDH11 attenuated the suppressive effect of an miR-27b inhibitor on cervical cancer cells. In addition, we found that CDH11 was involved in miR-27b-induced epithelial-mesenchymal transition (EMT) by regulating expression of E-cadherin, vimentin and N-cadherin. Our results for the first time indicate that miR-27b acting as an oncogene may play an important role in the progression of cervical cancer by modulating CDH11 and EMT.