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miR‐885‐5p plays an accomplice role in liver cancer by instigating TIGAR expression via targeting its promoter
Author(s) -
Zou Shubiao,
Rao Yao,
Chen Weicai
Publication year - 2019
Publication title -
biotechnology and applied biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.468
H-Index - 70
eISSN - 1470-8744
pISSN - 0885-4513
DOI - 10.1002/bab.1767
Subject(s) - expression (computer science) , liver cancer , biology , microbiology and biotechnology , cancer , cancer research , chemistry , genetics , computer science , programming language
Abstract TIGAR (TP53‐induced glycolysis and apoptosis regulator) is a p53‐inducible gene and its expression resulted in controlling metabolism and protection from apoptosis. Furthermore, TIGAR participated in promoting the pentose phosphate pathway and help in lowering intracellular reactive oxygen species. miR‐885‐5p has also been reported to be involved in liver tumorigenesis, but whether miR‐885‐5p has a regulatory effect on TIGAR expression is unknown. In this study, we found that their levels were correlated to each other and positively related to cell malignancy. Exogenous miR‐885‐5p induced TIGAR expression through a p53‐independent pathway. The promoter region of TIGAR harbors two tandem putative miR‐885‐5p target sites. Cotransfection of synthetic miR‐885 with TIGAR promoter reporter constructs significantly enhanced TIGAR promoter activity via binding with target sites. Furthermore, miR‐885‐5p and its precursor pre‐miR‐885 had the same stimulatory impact on TIGAR expression. Chromatin immunoprecipitation analysis further verified that increased miR‐885‐5p potentiated the accessibility of TIGAR promoter chromatin to transcriptional factors and facilitated TIGAR expression. miR‐885‐5p and its precursor both can interact mechanically with TIGAR promoter binding site and alter local chromatin structure, and subsequently upregulate TIGAR expression and participate in liver tumorigenesis.