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Overexpressing lncRNA SNHG16 inhibited HCC proliferation and chemoresistance by functionally sponging hsa-miR-93
Overexpressing lncRNA SNHG16 inhibited HCC proliferation and chemoresistance by functionally sponging hsa-miR-93
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Overexpressing lncRNA SNHG16 inhibited HCC proliferation and chemoresistance by functionally sponging hsa-miR-93
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Overexpressing lncRNA SNHG16 inhibited HCC proliferation and chemoresistance by functionally sponging hsa-miR-93
Overexpressing lncRNA SNHG16 inhibited HCC proliferation and chemoresistance by functionally sponging hsa-miR-93

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Overexpressing lncRNA SNHG16 inhibited HCC proliferation and chemoresistance by functionally sponging hsa-miR-93
Overexpressing lncRNA SNHG16 inhibited HCC proliferation and chemoresistance by functionally sponging hsa-miR-93
Journal Article

Overexpressing lncRNA SNHG16 inhibited HCC proliferation and chemoresistance by functionally sponging hsa-miR-93

2018
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Overview
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). 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. 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. Our data demonstrate that plays a critical role in HCC development via functionally sponging hsa-miR-93.