临床肿瘤学杂志 ›› 2018, Vol. 23 ›› Issue (5): 403-407.

• 论著 • 上一篇    下一篇

长链非编码RNA SNHG5在肝癌中表达及其对HepG2细胞增殖、凋亡的影响

  

  1. 1  515300  广东揭阳  普宁市人民医院肝胆胰外科
    2  510515  南方医科大学第一临床医学院
    3  510655  中山大学附属第六医院结直肠肛门外科
  • 收稿日期:2017-12-23 修回日期:2018-03-24 出版日期:2018-05-31 发布日期:2018-06-07
  • 基金资助:
    广东省医学科学技术研究基金项目(A2016164);广东省大学生攀登计划资助项目(pdjhb0111);国家级大学生创新创业训练计划资助项目(201712121034)

Preliminary study on the expression of long non-coding RNA SNHG5 hepatocellular carcinoma and its role in regulating proliferation and anti-apoptosis of HepG2 cell

  1. Department of Hepatobiliary and Pancreatic Surgery, Puning People’s Hospital, Jieyang 515300, China
  • Received:2017-12-23 Revised:2018-03-24 Online:2018-05-31 Published:2018-06-07

摘要: 目的   检测长链非编码RNA SNHG5在肝癌组织中的表达,并探讨其对肝癌HepG2细胞增殖、凋亡等生物学行为的调控作用与相关机制。方法   采用荧光定量PCR(QPCR)检测30例肝癌组织和对应癌旁组织中SNHG5的表达水平;采用小干扰RNA(siRNA)技术敲低肝癌HepG2细胞SNHG5的表达量,采用CCK-8法、流式细胞术、QPCR以及Western blotting检测HepG2细胞的增殖、凋亡情况以及凋亡通路相关标志物表达水平的变化。结果  肝癌组织中SNHG5的表达水平较其配对癌旁组织明显上调(P<0.05)。敲低SNHG5表达后HepG2细胞的增殖、抗凋亡能力均受到抑制,细胞凋亡蛋白cleaved caspase-3、BAX表达上调。结论  相较于正常组织,肝癌组织中长链非编码SNHG5呈高表达,SNHG5可能通过调节肝癌细胞的增殖、凋亡能力以及抑制凋亡通路激活进程而发挥促癌作用,可能是肝癌治疗的潜在靶点。

关键词: 肝癌, SNHG5, 增殖, 凋亡, caspase-3

Abstract:
【Abstract】Objective   To investigate the expression of lncRNA SNHG5 in hepatocellular carcinoma(HCC) tissues, and explore its biological regulation on cell proliferation and cell apoptosis. Methods   The mRNA expression level of SNHG5 in hepatocellular carcinoma tissues and adjacent normal tissues was determined by QPCR. Then HepG2 cells were transfected with siRNA to knockdown the expression of SNHG5. CCK-8, flow cytometry, QPCR and Western blotting were used to detect the biological characteristics of proliferation and apoptosis of HepG2 cells, as well as the changes in the expression level of apoptosis pathway related markers. Results  The expression level of SNHG5 in HCC tissues was significantly higher than that in matched adjacent tissues (P<0.05). After knocking down SNHG5 expression, the proliferation and anti-apoptotic ability of HepG2 cells were inhibited, and the expressions of apoptotic proteins cleaved caspase-3 and BAX were upregulated. Conclusion   SNHG5 was found to be overexpression in liver cancer tissues. SNHG5 might play as a potential therapeutic targetby regulating proliferation and apoptosis of HCC.


Key words: Hepatocellular carcinoma, SNHG5, Proliferation, Apoptosis, Caspase-3

中图分类号: 

  • R735.7
[1] 梁文昌, 郭荣平, 王俊生, 周 静.

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