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Aberrant expression of LncRNA‐MIR31HG regulates cell migration and proliferation by affecting miR‐31 and miR‐31* in Hirschsprung's disease
Author(s) -
Cai Peng,
Li Hongxing,
Huo Weiwei,
Zhu Hairong,
Xu Chao,
Zang Rujin,
Lv Wei,
Xia Yankai,
Tang Weibing
Publication year - 2018
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.26830
Subject(s) - downregulation and upregulation , microrna , cell growth , biology , microbiology and biotechnology , hek 293 cells , pi3k/akt/mtor pathway , long non coding rna , cancer research , gene , gene knockdown , signal transduction , genetics
Abstract Hirschsprung's disease (HSCR) is a birth defect that causes a failure of the enteric nervous system to cover the distal gut during early embryonic development. Evidence shows that long non‐coding RNAs (lncRNA) play important roles in HSCR. The MIR31 host gene (MIR31HG), also known as Loc554202, is a long non‐coding RNA (lncRNA), which acts as the host gene of (microRNA) miR‐31 and miR‐31*. There have been no studies regarding its function in early developmental defects during pregnancy, and its downstream genetic receptors. We report that downregulation of MIR31HG inhibited migration and proliferation in 293T and SH‐SY5Y cell lines, by suppressing miR‐31 and miR‐31*. Moreover, the downregulation of miR‐31 and miR‐31* enhanced inter‐α‐trypsin inhibitor heavy chain 5 (ITIH5) and the phosphatidylinositol‐4, 5‐bisphosphate 3‐kinase catalytic gamma subunit (PIK3CG), respectively with reductions of cell migration and proliferation in 293T and SH‐SY5Y cell lines. In addition, synergistic actions were observed between miR‐31 and miR‐31* in cell migration and proliferation. Our results demonstrated that the MIR31HG‐miR‐31/31*‐ITIH5/PIK3CG pathway plays a role in the pathogenesis of HSCR.