We found that miR-506 was significantly downregulated in human CC cell lines (HeLa and C33A) and clinical CC specimens as compared with matched cell lines and adjacent normal tissues, while the expression level of ABCC4 was higher in tumor tissues than it in adjacent normal tissues.
Overall, our study demonstrated that miR-506 inhibited the proliferation and EMT of cervical cancer cells by targeting FOXQ1 and provided evidence that the miR-506/FOXQ1 axis plays an important role in the pathogenesis of cervical cancer, representing potential molecular targets for the development of anticancer agents for cervical cancer treatment.