1. MicroRNA-200b inhibits epithelial-mesenchymal transition and migration of cervical cancer cells by directly targeting RhoE
- Author
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Min Hu, Feng Pan, Qi‑Fan Zhang, Bing‑Shu Li, Yan‑Xiang Cheng, Gan Tao Chen, and Chuang Chen
- Subjects
rho GTP-Binding Proteins ,0301 basic medicine ,Cancer Research ,Pathology ,medicine.medical_specialty ,Epithelial-Mesenchymal Transition ,Blotting, Western ,Cell ,Uterine Cervical Neoplasms ,Vimentin ,Biology ,Real-Time Polymerase Chain Reaction ,Biochemistry ,Metastasis ,03 medical and health sciences ,0302 clinical medicine ,Antigens, CD ,microRNA ,Genetics ,medicine ,Humans ,Epithelial–mesenchymal transition ,RNA, Small Interfering ,3' Untranslated Regions ,Molecular Biology ,Base Sequence ,Oncogene ,Oligonucleotides, Antisense ,Cell cycle ,Cadherins ,Actin cytoskeleton ,medicine.disease ,MicroRNAs ,030104 developmental biology ,medicine.anatomical_structure ,Oncology ,030220 oncology & carcinogenesis ,Cancer research ,biology.protein ,Molecular Medicine ,Female ,RNA Interference ,Sequence Alignment ,HeLa Cells - Abstract
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.
- Published
- 2016