Knockdown of the lncRNA SNHG8 inhibits cell growth in Epstein-Barr virus-associated gastric carcinoma

被引：42

作者：

Liu, Jing ^{[1
]}

Yang, Chunxia ^{[1
]}

Gu, Yufang ^{[2
]}

Li, Chong ^{[1
]}

Zhang, Huamei ^{[1
]}

Zhang, Wenfang ^{[1
]}

Wang, Xueqing ^{[1
]}

Wu, Nan ^{[1
]}

Zheng, Chunyan ^{[3
]}

机构：

[1] Dept Nephol, Zibo, Peoples R China

[2] Dept Gastrointestinal Surg, Zibo, Peoples R China

[3] Zibo Cent Hosp, Dept Med Care, 54 Gongqingtuan Rd, Zibo 255036, Shandong, Peoples R China

来源：

CELLULAR & MOLECULAR BIOLOGY LETTERS | 2018年 / 23卷

关键词：

SNHG8; Cell growth; shRNA; Epstein-Barr virus-associated gastric carcinoma; CANCER;

D O I：

10.1186/s11658-018-0070-8

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Background: Epstein-Barr virus (EBV) infection is causatively associated with a variety of human cancers, including gastric cancer (GC), which has one of the highest mortality rates of all human cancers. Long non-coding RNAs (lncRNAs) show important regulatory roles in human GC. SNHG8 is a recently identified lncRNA that was reported to show abnormal expression pattern in GC. However, little is known of its biological function in EBV-associated GC. Methods: We used cell viability, colony formation and cell cycle assays to investigate the roles of lncRNA SNHG8 in the cell growth of EBV-associated GC. Results: The transcript levels of SNHG8 in the cultured EBV-associated GC cells were significantly higher in the cultured EBV-associated GC cells compared with the levels in normal human gastric mucosal cells and EBV-negative GC cells. Knockdown of SNHG8 with specific shRNAs inhibited cell proliferation and colony formation and arrested the cell cycle in the G0/G1 phase in vitro. We also found that knockdown of SNHG8 suppressed tumor growth in vivo. Conclusions: These data indicate the pro-oncogenic potential of SNHG8 in sEBV-associated GC, meaning it is a latent therapeutic target for the treatment of this type of cancer.

引用

页数：10

共 22 条

[1] Inhibition. of medullary thyroid carcinoma cell proliferation and RET phosphorylation by tyrosine kinase inhibitors [J].