长链非编码RNA过表达通过功能性结合hsa-miR-93抑制肝癌细胞增殖和化疗耐药性。
Overexpressing lncRNA inhibited HCC proliferation and chemoresistance by functionally sponging hsa-miR-93.
作者信息
Xu Fengfeng, Zha Guoqing, Wu Yanpeng, Cai Weilong, Ao Jian
机构信息
Department of General Surgery, The Fifth Affiliated Hospital of Guangzhou Medical University, Guangzhou, People's Republic of China,
The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, People's Republic of China.
出版信息
Onco Targets Ther. 2018 Dec 7;11:8855-8863. doi: 10.2147/OTT.S182005. eCollection 2018.
BACKGROUND
Long noncoding RNAs (lncRNAs) have been identified as prognostic biomarkers and functional regulators in human cancers. The present study aimed to determine the expressions and functions of an lncRNA, (), in hepatocellular carcinoma (HCC).
PATIENTS AND METHODS
expressions were tested by quantitative real-time PCR (qRT-PCR) in HCC cell lines, as well as 43 pairs of HCC tissues and pair-matched healthy hepatic tissues. It was overexpressed in Hep3B and HuH7 cells. The effects of overexpression in HCC in vitro proliferation, 5-fluorouracil (5-FU) chemoresistance, and in vivo tumor growth were tested. A potential microRNA (miRNA) sponge target of , hsa-miR-93, was tested by luciferase reporter assay and qRT-PCR. In addition, hsa-miR-93 was upregulated in -overexpressed HCC cells to examine its effect on -mediated cancer cell functional regulation in HCC.
RESULTS
levels were markedly downregulated in both HCC cell lines and HCC tissues. Lentivirus-mediated overexpression inhibited HCC cell proliferation, 5-FU chemoresistance, and in vivo tumor growth. Hsa-miR-93 was confirmed to be directly sponging on . Its upregulation in HCC cells reversed overexpression and induced tumor-suppressing effects in HCC cells.
CONCLUSION
Our data demonstrate that plays a critical role in HCC development via functionally sponging hsa-miR-93.
背景
长链非编码RNA（lncRNAs）已被确定为人类癌症中的预后生物标志物和功能调节因子。本研究旨在确定一种lncRNA，（此处原文缺失具体名称），在肝细胞癌（HCC）中的表达及功能。
患者与方法
通过定量实时PCR（qRT-PCR）检测HCC细胞系以及43对HCC组织和配对的健康肝组织中（此处原文缺失具体名称）的表达。在Hep3B和HuH7细胞中过表达（此处原文缺失具体名称）。检测（此处原文缺失具体名称）过表达对HCC体外增殖、5-氟尿嘧啶（5-FU）化疗耐药性及体内肿瘤生长的影响。通过荧光素酶报告基因检测和qRT-PCR检测（此处原文缺失具体名称）潜在的微小RNA（miRNA）海绵靶点hsa-miR-93。此外，在（此处原文缺失具体名称）过表达的HCC细胞中上调hsa-miR-93，以检测其对HCC中（此处原文缺失具体名称）介导的癌细胞功能调节的影响。
结果
在HCC细胞系和HCC组织中（此处原文缺失具体名称）水平均显著下调。慢病毒介导的（此处原文缺失具体名称）过表达抑制了HCC细胞增殖、5-FU化疗耐药性及体内肿瘤生长。证实hsa-miR-93直接靶向（此处原文缺失具体名称）。其在HCC细胞中的上调逆转了（此处原文缺失具体名称）过表达并诱导了HCC细胞中的肿瘤抑制作用。
结论
我们的数据表明，（此处原文缺失具体名称）通过功能性靶向hsa-miR-93在HCC发展中起关键作用。
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