Open Access

ARTICLE

MicroRNA-520b Functions as a Tumor Suppressor in Colorectal Cancer by Inhibiting Defective in Cullin Neddylation 1 Domain Containing 1 (DCUN1D1)

Jing Xiao^*, Guang Li^†, Jingyu Zhou^‡, Shalong Wang^‡, Dongcai Liu^‡, Guoshun Shu^‡, Jianping Zhou^‡, Feng Ren^‡

* Minimally Invasive Surgery Center, The Second Xiangya Hospital of Central South University, Changsha, Hunan, P.R. China
† Department of Gastrointestinal Surgery, People’s Hospital of Linyi City, Linyi, Shandong, P.R. China
‡ Department of Gerontological Surgery, The Second Xiangya Hospital of Central South University, Changsha, Hunan, P.R. China

Oncology Research 2018, 26(4), 593-604. https://doi.org/10.3727/096504017X14920318811712

Abstract

MicroRNAs (miRs), a class of small noncoding RNAs, are important regulators for gene expression through directly binding to the 3'-untranslated region (3'-UTR) of their target mRNA. Recently, downregulation of miR-520b has been observed in several common human cancers. However, the exact role of miR-520b in colorectal cancer (CRC) has not previously been studied. In this study, our data showed that miR-520b was significantly downregulated in CRC and cell lines when compared with adjacent normal tissues and a normal intestinal epithelial cell line. Low expression of miR-520b was notably associated with the malignant progress and a shorter survival time for CRC patients. Restoration of miR-520b inhibited cell proliferation, migration, invasion, and epithelial–mesenchymal transition (EMT) in CRC cells. Defective in cullin neddylation 1 domain containing 1 (DCUN1D1) was then identified as a novel target gene of miR-520b in CRC cells. The expression of DCUN1D1 was significantly increased in CRC, with a negative correlation to miR-520b expression in CRC tissues. Moreover, a high expression of DCUN1D1 was significantly associated with the malignant progress and a poor prognosis for CRC patients. Furthermore, overexpression of DCUN1D1 rescued the miR- 520b-mediated malignant phenotypes and EMT in CRC cells. The data demonstrate that miR-520b functions as a tumor suppressor in CRC through targeting DCUN1D1, suggesting that miR-520b may become a potential therapeutic target for the treatment of CRC.

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