Long non-coding RNA linc-ITGB1 promotes cell proliferation and migration in human hepatocellular carcinoma cells

被引:10
|
作者
Shang, Meiling [1 ]
Xu, Xinhua [1 ]
Zhang, Min [1 ]
Yang, Hongyuan [1 ]
机构
[1] Weifang Peoples Hosp, Dept Infect Dis, 151 Guangwen St, Weifang 261000, Shandong, Peoples R China
关键词
linc-ITGB1; hepatocellular carcinoma; proliferation; migration; invasion; INVASION; GROWTH; METASTASIS; LINKS; GENE;
D O I
10.3892/etm.2017.5143
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Hepatocellular carcinoma (HCC) represents a major endpoint of chronic liver diseases and is the third leading cause of cancer-related mortality. Long intergenic non-coding RNA-integrin subunit beta 1 ITGB1 (linc-ITGB1) is a novel long non-coding RNA, which is implicated in the development and progression of human tumors. However, its involvement in hepatocarcinogenesis remains to be elucidated. In the present study, the specific roles of linc-ITGB1 on cell proliferation and metastasis in HCC were investigated. It was initially observed that the expression of linc-ITGB1 was significantly elevated in 30 cases of clinical HCC tissues relative to their adjacent non-cancerous tissues. Expression of linc-ITGB1 was particularly elevated in the highly invasive cell line, HCCLM3. Knockdown of linc-ITGB1 in HCCLM3 cells using a specific short hairpin RNA decreased cell viability and colony formation in vitro. In addition, cell cycle analysis demonstrated that linc-ITGB1-depleted cells accumulated in the G0/G1 phase. HCCLM3 cells with linc-ITGB1 depletion exhibited significantly decreased migration and invasion abilities, when compared with control cells (P<0.05). These data suggest that linc-ITGB1 promotes HCC progression by inducing cell-cycle arrest. Therefore, targeted therapy against linc-ITGB1 may be a novel strategy to treat HCC.
引用
收藏
页码:4687 / 4692
页数:6
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