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Disease Markers
Volume 2017 (2017), Article ID 2827435, 8 pages
https://doi.org/10.1155/2017/2827435
Research Article

miR-202 Suppresses Cell Proliferation by Targeting FOXR2 in Endometrial Adenocarcinoma

Department of Obstetrics and Gynecology, The 2nd Hospital of Shandong University, Jinan, Shandong 250012, China

Correspondence should be addressed to Hui Xu

Received 5 March 2017; Revised 6 June 2017; Accepted 18 June 2017; Published 30 July 2017

Academic Editor: Matteo Giulietti

Copyright © 2017 Xinchao Deng et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Background. MicroRNA-202 (miR-202) has been reported to be aberrantly regulated in several cancers. The aim of this study is to explore the functional role of miR-202 in EAC tumor growth. Material and Methods. miR-202 expression was detected by qRT-PCR. TargetScan and luciferase reporter assay were used to elucidate the candidate target gene of miR-202. The FOXR2 protein level was assessed by Western blot and immunohistochemistry. Survival analysis was explored for FOXR2 expression in EAC patients. Results. miR-202 expression was significantly decreased in EAC tissues () compared with that in control tissues. And the downregulate miR-202 was significantly associated with poor prognosis (). Re-expression of miR-202 dramatically suppressed cell proliferation in vitro and tumor growth in vivo. FOXR2 was identified as a direct target of miR-202. In EAC tissues, FOXR2 was upregulated and the increased FOXR2 was significantly associated with poor prognosis. In miR-202-transfected cells, the FOXR2 expression was inversely changed. The analysis of FOXR2 protein expression and miR-202 transcription in EAC tissues showed negative correlation (). Conclusion. miR-202 may function as a tumor suppressor in EAC tumor growth by targeting FOXR2 oncogene, which may provide new insights into the molecular mechanism and new targets for treatment of EAC.