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Long non‐coding RNA ANRIL enhances mitochondrial function of hepatocellular carcinoma by regulating the MiR‐199a‐5p/ARL2 axis
Author(s) -
Li Kun,
Zhao Bao,
Wei Diandian,
Cui Yixuan,
Qian Lisheng,
Wang Wenrui,
Liu Guodong
Publication year - 2020
Publication title -
environmental toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.813
H-Index - 77
eISSN - 1522-7278
pISSN - 1520-4081
DOI - 10.1002/tox.22867
Subject(s) - gene knockdown , long non coding rna , mitochondrion , microbiology and biotechnology , mitochondrial dna , reprogramming , microrna , cancer research , biology , rna , cell , chemistry , gene , biochemistry
Although the roles of long non‐coding RNA (lncRNA) ANRIL (Antisense non‐coding RNA in the INK4A locus) have been established in various tumors, its roles in mitochondrial metabolic reprogramming of hepatocellular carcinoma (HCC) cells are still unclear. This work aims to explore lncRNA ANRIL roles in regulating the mitochondrial metabolic reprogramming of liver cancer cells. First, we found that lncRAN ANRIL expression was significantly increased in HCC tissues or cells compared with the normal adjacent tissues and normal tissues or cells. Functional experiment showed that overexpression of lncRNA ANRIL promoted mitochondrial function in HCC cells, evident by the increased mitochondrial DNA copy numbers, ATP (Adenosine triphosphate) level, mitochondrial membrane potential, and the expression levels of mitochondrial markers, while ANRIL knockdown exerted the opposite effects. Mechanistically, lncRNA ANRIL acted as a competing endogenous RNA to increase ARL2 (ADP‐ribosylationfactor‐like 2) expression via sponging miR‐199a‐5p. Notably, the miR‐199a‐5p/ARL2 axis is necessary for ANRIL‐mediated promoting effects on HCC cell mitochondrial function. This work reveals a novel ANRIL‐miR‐199a‐5p‐ARL2 axis in HCC cell progression, which might provide potential targets for HCC treatment.