MiR-139-5p-ZEB1 is a Molecular Regulator of Growth, Invasion, and Epithelial-to-Mesenchymal Transition of Cervical Cancer

Objective: To verify that miR-139-5p-zinc finger E-box-binding homeobox 1 (ZEB1) is a molecular regulator of the biological function and epithelial-mesenchymal transition (EMT) of cervical cancer (CC) cells. Methods: Cancerous tissues, corresponding paracancerous tissues, and serum were sampled from patients with CC. MiR-139-5p and ZEB1 in tissue specimens, serum specimens, and purchased CC cell lines were quantified, and Pearson correlation coefficient was adopted for correlation analysis of miR-139-5p in clinical specimens. Receiver operating characteristic (ROC) curves were adopted to analyze the diagnostic value of miR-139-5p and ZEB1 for CC. The expression of genes in CC cells was changed by transfection. The proliferation, colony formation, invasion, and apoptosis of cells were determined, and the protein level of EMT markers (N-cadherin, vimentin, and E-cadherin) was also quantified. Moreover, the targeting relationship between miR-139-5p and ZEB1 was determined. Results: Our data showed that the expression of miR-139-5p decreased greatly in CC tissues, and it also significantly decreased in the serum, while the expression of serum ZEB1 was opposite. In addition, the miR-139-5p expression in CC tissues was positively correlated with that in serum, while serum miR-139-5p was negatively correlated with serum ZEB1. The areas under the curves (AUCs) of the two for identifying CC were 0.923 and 0.890, respectively. Both up-regulation of miR-139-5p and down-regulation of ZEB1 suppressed the colony formation, proliferation, invasion, and EMT of CC cells, and intensified their apoptosis. Moreover, miR-139-5p negatively regulated the transcription of ZEB1, and down-regulation of the former could reverse the molecular regulatory effects of down regulating ZEB1 on the above biological behaviors of CC cells. Conclusion: The above data imply that miR-139-5p-ZEB1 axis may be the key to curbing the progression of CC.