Open Access

ARTICLE

miR-133a-3p Targets SUMO-Specific Protease 1 to Inhibit Cell Proliferation and Cell Cycle Progress in Colorectal Cancer

Guo-Qiang Zhou^*, Fu Han^*, Zhi-Liang Shi^*, Liang Yu^*, Xue-Feng Li^*, Cheng Yu^*, Cheng-Long Shen^*, Dai-Wei Wan^†, Xin-Guo Zhu^†, Rui Li^‡, Song-Bing He^†

* Department of Gastrointestinal Surgery, Changshu No. 2 Hospital, Suzhou, P.R. China
† Department of General Surgery, The First Affiliated Hospital of Soochow University, Suzhou, P.R. China
‡ Department of Gastroenterology, The First Affiliated Hospital of Soochow University, Suzhou, P.R. China

Oncology Research 2018, 26(5), 795-800. https://doi.org/10.3727/096504017X15004613574679

Abstract

Dysregulation of SUMO-specific protease 1 (SENP1) expression has been reported in several kinds of cancer, including human colorectal and prostate cancers, proposing SENP1 as an oncogene with a critical role in cancer progression. miR-133a-3p has been reported as a tumor suppressor in several malignant neoplasias. However, the precise molecular mechanisms underlying its role in colorectal cancer remain largely unknown. The aim of this work was to investigate the relationship between miR-133a-3p and SENP1 in colorectal cancer cells. We found that miR-133a-3p expression was downregulated in colorectal cancer tissues. In silico analyses indicated that SENP1 is one of the target genes of miR-133a-3p. Overexpression of miR-133a-3p mimics was able to inhibit cell growth with G1 arrest of colorectal cancer cells. Overexpression of miR-133a-3p antisense promoted cell growth of colorectal cancer cells. The luciferase reporter experiments showed that miR-133a-3p regulated the expression of SENP1 by combining with its 3'-UTR and resulted in downregulation of SENP1 and upregulation of CDK inhibitors such as p16, p19, p21, and p27. These results suggest that the miR-133a- 3p–SENP1 axis might play a role in cell proliferation and cell cycle regulation of colorectal cancer cells.

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