Effect of miR-483-3p on DLC1 Expression in Colorectal Cancer
10.3969/j.issn.1008-7125.2014.07.003
- VernacularTitle:miR-483-3 p对结直肠癌DLC1基因表达的影响
- Author:
Jingrui JIANG
;
Yuan LIU
;
Shaogen WU
;
Wangsen CAO
;
Hengmi CUI
;
Chenggong YU
- Publication Type:Journal Article
- Keywords:
MicroRNA-483-3p;
DeletedinLiverCancer1;
ColorectalNeoplasms;
Epigenetics;
Cell Proliferation
- From:
Chinese Journal of Gastroenterology
2014;(7):394-398
- CountryChina
- Language:Chinese
-
Abstract:
Background:Suppression of tumor suppressor genes plays a key role in the pathogenesis and progress of tumors. Some microRNAs may contribute to tumorigenesis by regulating tumor suppressor genes. Aims:To investigate the targeted regulatory effect of miR-483-3p on deleted in liver cancer 1(DLC1)gene in colorectal cancer. Methods:Sixteen patients with colorectal cancer admitted from October 2012 to April 2013 at Nanjing Drum Tower Hospital were enrolled. Expression of DLC1 in cancerous and adjacent noncancerous tissues was determined by Western blotting,and expression of miR-483-3p was determined by qRT-PCR. Dual luciferase reporter gene plasmid containing the 3’untranslated region(3’UTR)of DLC1 was constructed to validate the regulation of DLC1 by miR-483-3p in human colon cancer cell line HCT116. MiR-483-3p mimic was transfected into HEK293T cells and expression of DLC1 was determined by Western blotting;MiR-483-3p mimic was transfected into HCT116 cells and cell proliferation was measured by CCK-8 assay. Results:Expression of DLC1 was significantly lower in cancerous tissue than in noncancerous tissue,while expression of miR-483-3p was significantly higher in cancerous tissue than in noncancerous tissue(P<0. 05). MiR-483-3p mimic reduced the expression of DLC1 through directly binding to the 3’UTR of DLC1. Transfection of miR-483-3p mimic enhanced the proliferation of HCT116 cells significantly(P<0. 05). Conclusions:DLC1 is a target gene of miR-483-3p. MiR-483-3p might promote the development of colorectal cancer by down-regulating DLC1 expression at post-transcriptional level.
