Lentivirus-mediated silencing of SCIN inhibits proliferation of human lung carcinoma cells

被引:21
|
作者
Liu, Hongxu [1 ]
Shi, Daiwang [1 ]
Liu, Tieqin [1 ]
Yu, Zhanwu [2 ]
Zhou, Chuanjiang [3 ]
机构
[1] China Med Univ, Hosp 1, Dept Thorac Surg, Shenyang 110001, Peoples R China
[2] Liaoning Canc Hosp & Inst, Dept Thorac Surg, Shenyang 110042, Peoples R China
[3] Benxi Cent Hosp, Dept Thorac Surg, Benxi 117000, Peoples R China
基金
中国国家自然科学基金;
关键词
SCIN; Lentivirus; RNAi; Proliferation; Lung carcinoma; CANCER-CELLS; ACTIN CYTOSKELETON; CHROMAFFIN CELLS; APOPTOSIS; SCINDERIN; EXPRESSION; DIFFERENTIATION; EXOCYTOSIS; ADSEVERIN; INVASION;
D O I
10.1016/j.gene.2014.10.013
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
SCIN (scinderin) is a calcium-dependent actin severing and capping protein. Homologue in zebrafish has been found to be related with cell death. In the present study, we found that SCIN is highly expressed in human lung cancer specimens. However, the role of SCIN in lung cancer has not yet been determined. To investigate the function of SCIN in lung carcinoma cells, we took advantage of lentivirus-mediated RNA interference (RNAi) to knockdown SCIN expression in two lung carcinoma cell lines A549 and H1299. Silencing of SCIN significantly inhibited the proliferation and colony formation ability of both cell lines in vitro. Moreover, flow cytometry analysis showed that knockdown of SCIN led to G0/G1 phase cell cycle arrest as well as an excess accumulation of cells in the sub-G1 phase. Furthermore, depletion of SCIN resulted in a significant increase in Cyclin B1, p21 and PARP expression, and a little decrease in Cyclin D1 expression. These results suggest that SCIN plays an important role in lung carcinoma cell proliferation, and lentivirus-mediated silencing of SCIN might be a potential therapeutic approach for the treatment of lung-cancer. (C) 2014 Elsevier B.V. All rights reserved.
引用
收藏
页码:32 / 39
页数:8
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