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MiR-718 mediates the indirect interaction between lncRNA SEMA3B-AS1 and PTEN to regulate the proliferation of hepatocellular carcinoma cells
Author(s) -
Yuchuan Zhong,
Yan Li,
Tao Song,
Dapeng Zhang
Publication year - 2019
Publication title -
physiological genomics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.078
H-Index - 112
eISSN - 1531-2267
pISSN - 1094-8341
DOI - 10.1152/physiolgenomics.00019.2019
Subject(s) - tensin , pten , biology , hepatocellular carcinoma , cancer research , downregulation and upregulation , cancer , carcinoma , apoptosis , gene , pi3k/akt/mtor pathway , genetics
It has been reported that SEMA3B-AS1 is a tumor-suppressive lncRNA in gastric cardia adenocarcinoma. We explored the possible involvement of SEMA3B-AS1 in hepatocellular carcinoma (HCC). We found that SEMA3B-AS1 was downregulated in HCC tissues compared with noncancer tissues and was not affected by hepatitis B virus (HBV) and hepatitis C virus (HCV) infections. In addition, SEMA3B-AS1 expression was not affect by cancer development, and low SEMA3B-AS1 levels were closely correlated with poor survival. SEMA3B-AS1 in HCC tissues was inversely correlated with microRNA (miR)-718 and positively correlated with PTEN. In HCC cells, SEMA3B-AS1 overexpression resulted in upregulated, while miR-718 overexpression resulted in downregulated phosphatase and tensin homolog (PTEN) expression. In addition, miR-718 overexpression attenuated the effects of SEMA3B-AS1 overexpression. SEMA3B-AS1 and PTEN overexpression resulted in a reduced proliferation rate of HCC cells, while miR-718 overexpression resulted in an increased rate. In addition, miR-718 overexpression attenuated the effects of SEMA3B-AS1 overexpression. Therefore, miR-718 may mediate the indirect interaction between lncRNA SEMA3B-AS1 and PTEN to regulate the proliferation of hepatocellular carcinoma cells.

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