MiR-630 acts as a tumor suppressor in cervical cancer and inhibits epithelial-mesenchymal transition in cervical cancer

Metastasis and recurrence are the main causes of death in advanced cervical cancer patients. E6/E7, the early genes of the high-risk mucosal human papillomavirus type, plays vital roles in the carcinogenic process of cervical cancer. Beyond this, multifactor can contribute to the formation and evolution of cervical cancer, among which miRNAs play an important role in cancer development and progression. In this study, we found that E6/ E7 could remarkably regulate several miRNAs via miRNA microarray analysis. Among these miRNAs negatively regulated by E6/E7, we highlighted the function and molecular mechanism of miR-630 in cervical cancer. We first identified miR-630 expression status in a screen of 10 cervical cancer tissues and matched normal tissues, and found that miR-630 was significantly decreased in tumor tissues compared to normal tissues. Further experiments showed that alteration of miR-630 expression had profound impact on cellular migration and invasion efficiency, down-regulation of miR-630 increased invasion and migration capacity of cancer cells, while overexpression of miR630 obtained the opposite result. RT-PCR and western blotting analysis demonstrated that miR-630 inhibit EMT in cervical cancer. Further we proved p53 can positively regulate miR-630 expression in cervical cancer cells through CHIP assay. Taken together, miR-630 might act as a tumor suppressor in cervical cancer and inhibit migration and invasion ability of cervical cancer cells through regulating EMT. Moreover, miR-630 expression could be regulated by E6/E7-p53 signaling pathway.