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Long noncoding RNA DLGAP1‐AS1 promotes cell proliferation in hepatocellular carcinoma via sequestering miR‐486‐5p
Author(s) -
Peng Xiaochun,
Wei Fengmei,
Hu Xiaoli
Publication year - 2020
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.29430
Subject(s) - gene knockdown , cancer research , long non coding rna , cell growth , ectopic expression , downregulation and upregulation , biology , hepatocellular carcinoma , cell , antisense rna , competing endogenous rna , cell culture , gene silencing , rna , gene , genetics
Hepatocellular carcinoma (HCC) is most prevalent tumor in liver and one of the most fatal cancers in the world. Long noncoding RNAs (lncRNAs) have been accepted as important regulators in carcinomas. But there are still many lncRNAs including DLGAP1‐AS1 unannotated in HCC. First of all, GEPIA suggested that DLGAP1‐AS1 presented high expression in HCC tissue samples relative to the normal tissues. Besides, overexpression of DLGAP1‐AS1 was also proved in HCC cell lines. Moreover, DLGAP1‐AS1 knockdown efficiently suppressed cell proliferation in HCC. Interestingly, miR‐486‐5p was predicted and validated to interact with DLGAP1‐AS1, while the level of miR‐486‐5p was significantly increased In HCC after DLGAP1‐AS1 knockdown. Moreover, we uncovered that ectopic expression of miR‐486‐5p induced suppression on HCC cell proliferation and that miR‐486‐5p inhibition offset the effect of DLGAP1‐AS1 silence on HCC cell proliferation and apoptosis. Furthermore, H3F3B was identified as target of miR‐486‐5p and was therefore positively regulated by DLGAP1‐AS1 in HCC. Of note, H3F3B upregulation partly revived the declined cell proliferative capacity in response to DLGAP1‐AS1 knockdown. To conclude, DLGAP1‐AS1 exerted its oncogenic role in HCC via miR‐486‐5p/H3F3B axis. Our new findings provided novel theoretical basis for discovery of therapeutic targets of HCC.