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

被引:36
|
作者
Zhou, Guo-Qiang [1 ]
Han, Fu [1 ]
Shi, Zhi-Liang [1 ]
Yu, Liang [1 ]
Li, Xue-Feng [1 ]
Yu, Cheng [1 ]
Shen, Cheng-Long [1 ]
Wan, Dai-Wei [2 ]
Zhu, Xin-Guo [2 ]
Li, Rui [3 ]
He, Song-Bing [2 ]
机构
[1] Changshu 2 Hosp, Dept Gastrointestinal Surg, Suzhou, Peoples R China
[2] Soochow Univ, Dept Gen Surg, Affiliated Hosp 1, 188 Shizi St, Suzhou 215006, Jiangsu, Peoples R China
[3] Soochow Univ, Dept Gastroenterol, Affiliated Hosp 1, Suzhou, Peoples R China
关键词
Colorectal cancer; miR-133a-3p; SUMO-specific protease 1 (SENP1); CDK inhibitors; MICRORNAS; IDENTIFICATION; BIOMARKERS; HYPOXIA;
D O I
10.3727/096504017X15004613574679
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
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 G(1) 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.
引用
收藏
页码:795 / 800
页数:6
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