MicroRNA-200b inhibits epithelial-mesenchymal transition and migration of cervical cancer cells by directly targeting RhoE

Previous studies have identified microRNA-200b (miR-200b) as a powerful regulator of epithelial-mesenchymal transition (EMT) via the control of gene expression. EMT is a critical event that is associated with the initiation of malignant tumor metastasis. A lack of E-cadherin expression and overexpression of vimentin are hallmarks of EMT. It is well-known that RhoE, which is associated with regulation of the actin cytoskeleton and migration via alterations in cell motility, regulates the expression of E-cadherin, matrix metalloproteinase-9 (MMP-9) and vimentin. However, it remains to be elucidated whether miR-200b may alter the molecular behavior of RhoE. The present study aimed to determine whether miR-200b was able to regulate the EMT of cervical cancer, in order to control metastasis. In addition, the correlation between miR-200b and RhoE, E-cadherin and vimentin expression was investigated. Notably, miR-200b was shown to inhibit the function of RhoE and suppress the EMT of cervical cancer. Furthermore, HeLa cells were transfected with miR-200b mimics or inhibitors, and the protein expression levels of E-cadherin, MMP-9, vimentin and RhoE were subsequently detected. A Transwell assay was also conducted, in order to observe the metastatic ability of the HeLa cells. In addition, a luciferase reporter assay was performed using luciferase reporter vectors containing the full length 3'-untranslated region (UTR) of RhoE; miR-200b was able to significantly suppress relative luciferase activity by targeting the 3'-UTR of RhoE. These results suggested that miR-200b may markedly inhibit metastatic potential by regulating cell EMT and inhibiting RhoE; therefore, miR-200b may be considered an effective target for the treatment of patients with highly metastatic cervical cancer.