The interactions between MicroRNA-200c and BRD7 in endometrial carcinoma
- Park, Young-Ae; Lee, Jeong-Won; Choi, Jung-Joo; Jeon, Hye-Kyung; Cho, YoungJae; Choi, ChelHun; Kim, Tae-Joong; Lee, Nak Woo; Kim, Byoung-Gie; Bae, Duk-Soo
- Issue Date
- ACADEMIC PRESS INC ELSEVIER SCIENCE
- MicroRNA; Endometrial carcinoma; MicroRNA-200c; BRD7; beta-catenin
- GYNECOLOGIC ONCOLOGY, v.124, no.1, pp.125 - 133
- Journal Title
- GYNECOLOGIC ONCOLOGY
- Start Page
- End Page
- Objective. Increased expression of miR-200c was recently reported in endometrial carcinoma compared with normal tissues. In this study, we evaluated the role of miR-200c in cell growth and drug sensitivity in endometrial carcinoma and investigated the underlying mechanisms. Methods. The expression of miR-200c in human endometrial tissues was detected by quantitative RT-PCR. The transfection with anti-miRNA (anti-miR) or the premature form of miRNA (pre-miR) was performed to regulate the level of expression of miRNA-200c in enclometrial carcinoma cells, HEC-1A and Ishikawa. To identify the target genes for miR-200c, we performed mRNA microarray after pre-miR-200c transfection in HEC-1A cells. Results. We found that miR-200c expression was increased in enclometrial carcinoma compared with normal endometrial tissues. Anti-miR or pre-miR-200c could regulate cell survival, proliferation, and apoptosis and affect cytotoxicity in endometrial cancer cells. Through mRNA microarray analysis, we found that miR-200c inhibits the expression of BRD7, which was recently reported as a potential tumor suppressor gene. MiR-200c regulated the translocation of beta-catenin from the cytoplasm to the nucleus via inhibition of BRD7, resulting in increased expression of its transcriptional target genes, cyclinD1 and c-myc. Conclusion. The interaction between miR-200c and BRD7 slight have important roles in controlling growth of endometrial of cancer cells and suggest a novel target pathway for treatment of this cancer.(C) 2011 Elsevier Inc. All rights reserved.
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- 2. Clinical Science > Department of Obstetrics and Gynecology > 1. Journal Articles
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