Journal
MOLECULAR MEDICINE REPORTS
Volume 13, Issue 4, Pages 3139-3146Publisher
SPANDIDOS PUBL LTD
DOI: 10.3892/mmr.2016.4933
Keywords
epithelial-mesenchymal transition; microRNA-200b; RhoE; cervical cancer
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Funding
- Natural Science Foundation of China [81302273, 81201196]
- Science and Technology Department of Hubei Province, China [ZRY039]
- Health and Family Planning Commission of Hubei Province, China [2012ZY02]
- Chinese Postdoctoral Science Foundation [2011M500857]
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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.
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