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Journal of biosciences · Dec 2019
MiR-195 inhibits migration, invasion and epithelial-mesenchymal transition (EMT) of endometrial carcinoma cells by targeting SOX4.
- Xiaomeng Zhao, Lili Dai, Qifang Yue, Hua Wang, X U Wang, Yuan Li, and Ran Chen.
- Department of Gynecology and Obstetrics, The Shijiazhuang Cardiovascular Hospital, Shijiazhuang, Hebei, China.
- J. Biosci. 2019 Dec 1; 44 (6).
AbstractMicroRNAs (miRNAs) have been identified as potential biomarkers for endometrial carcinoma (EC) diagnosis, prognosis and therapy. The purpose of the present study was to investigate the detailed role and molecular mechanism of miR-195 in EC metastasis. qRT-PCR assay was performed to assess the expression of miR-195 and SRY-related high-mobility group box 4 (SOX4) mRNA in EC tissues and cells. The levels of N-cadherin, Vimentin, E-cadherin and SOX4 protein were determined by western blot. SOX4 protein expression in EC tissues was also determined by Immunohistochemistry (IHC) experiment. Transwell assay was used to analyze cell migration and invasion abilities. Dual-luciferase reporter assay and RNA Immunoprecipitation (RIP) assay were performed to confirm the targeted interaction between miR-195 and SOX4. Our data supported that miR-195 was downregulated and SOX4 was upregulated in EC tissues and cell lines. Upregulation of miR-195 inhibited migration, invasion and epithelial-mesenchymal transition (EMT) of EC cells. Moreover, SOX4 was a direct target of miR-195. MiR-195 overexpression-mediated anti-migration, anti-invasion and anti-EMT effects were antagonized by SOX4 restoration in EC cells. In conclusion, our study suggested that miR-195 inhibited the migration, invasion and epithelial mesenchymal transition (EMT) of EC cells at least partly by targeting SOX4. Our study provided a novel underlying mechanism for EC metastasis and a promising therapeutic target for EC management.
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