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.
Keywords: MicroRNAs; NR2F2; colorectal cancer; miR-382.
© 2016 Wiley Periodicals, Inc.