期刊
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
卷 398, 期 1, 页码 1-6出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2010.05.082
关键词
miR-331-3p; Gastric cancer; Growth arrest; E2F1
资金
- Chinese National High Tech Program [863-2006AA02A402, 863-2006AA 02A301]
- National Natural Science Foundation of China [30770961, 30973486, 30670939]
- Shanghai Pu Jiang Project [PJ200700367]
- Shanghai Science and Technology Commission [09JC1409600, 09DZ1950101]
- Shanghai Charity Foundation for Cancer Research
Deregulation of E2F1 activity is characteristic of gastric tumorigenesis, which involves in complex molecular mechanisms. microRNA is one of the post-transcriptional regulators for gene expression. Here, we report a member of miR-331 family, miR-331-3p, which was decreased in some kinds of malignancies. However, the biological function of miR-331-3p on gastric cancer is largely unknown. In this study, we screened the expressing levels of miR-331-3p and E2F1 in gastric cancer cell lines. We transfected precursor or inhibitor of miR-331-3p into gastric cancer cells. As results, miR-331-3p is down-regulated in all gastric cancer cell lines by real-time PCR. Over-expression of miR-331-3p blocked G1/S transition on SGC-7901 and AGS cell lines. Introduction of miR-331-3p dramatically suppressed the ability of colony formation and cell growth in vitro by interfering E2F1 activity. Our data highlight an important role of miR-331-3p in cell cycle control by targeting 3'-UTR of cell cycle-related molecule E2F1. We concluded that miR-331-3p is a potential tumor suppressor in gastric cancer. Restoring miR-331-3p in gastric cancer cells revealed potential application in gastric cancer therapy. (C) 2010 Published by Elsevier Inc.
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