MiR‐382 inhibits cell growth and invasion by targeting NR2F2 in colorectal cancer. Issue 12 (22nd January 2016)

• Record Type: Journal Article
• Authors: Zhou, Baoguo; Song, Jianwei; Han, Taotao; Huang, Mingkui; Jiang, Hongpeng; Qiao, Haiquan; Shi, Juan; Wang, Yuli
• Is Part Of: Molecular carcinogenesis. Volume 55:Issue 12(2016:Dec.)
• Page Start: 2260
• Page End: 2267
• Publication Date: 2016-01-22
• Subjects: colorectal cancer -- MicroRNAs -- miR‐382 -- NR2F2; Carcinogenesis -- Molecular aspects -- Periodicals; 616.994071
• DOI: 10.1002/mc.22466
• Languages: English
• ISSNs: 0899-1987

Abstract

Abstract : Colorectal cancer (CRC) is one of the leading causes of cancer death worldwide. MiR‐382 has been found to have a decreased expression and the ability to suppress tumorigenesis in certain cancers. However, the role of miR‐382 in CRC has not been sufficiently investigated. NR2F2 (also known as COUP‐TFII), a member of the steroid/thyroid receptor superfamily, is often aberrantly activated in various tumors, but it is currently unclear whether NR2F2 may be a target of miR‐382. In the present study, we investigated the role of miR‐382 in CRC and identified the regulation of NR2F2 by miR‐382. We observed that miR‐382 was aberrantly downregulated in CRC. Transfection with miR‐382 mimics impeded the growth, migration, and invasion of CRC cells. The direct binding of miR‐382 to the 3′ untranslated region (3′ UTR) of NR2F2 was confirmed using a luciferase reporter gene assay. We showed that the relative expression levels of NR2F2 were significantly higher in CRC tissues compared with normal adjacent mucosa. A Kaplan–Meier analysis indicated that patients with high NR2F2 expression had a poor overall survival. Knockdown of NR2F2 inhibited CRC cell growth, migration, and invasion. Ectopic expression of NR2F2 mitigated miR‐382 suppression of CRC cell proliferation, migration, and invasion. In conclusion, the present study describes a potential mechanism underlying a miR‐382/NR2F2 link contributing to CRC development. Our results demonstrate that miR‐382 represents a potential strategy against CRC. © 2016 Wiley Periodicals, Inc.