Open AccessLipopolysaccharide enhances ADAR 2 which drives Hirschsprung's disease by impairing miR‐142‐3p biogenesis
Author(s) -
Peng Lei,
Zhang Hua,
Su Yang,
Shen Qiyang,
Du Chunxia,
Xie Hua,
Li Hongxing,
Yan Jin,
Shen Ziyang,
Jiang Weiwei,
Xia Yankai,
Xu Xiaoqun,
Tang Weibing
Publication year - 2018
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.13652
Subject(s) - adar , rna editing , rna , biology , microrna , microbiology and biotechnology , lipopolysaccharide , rna binding protein , transcriptome , cancer research , gene expression , immunology , biochemistry , gene
Researches over the past decade suggest that lipopolysaccharide is a dominant driver of gastrointestinal motility and could damage the enteric neuron of rat or porcine. However, it remains poorly defined whether LPS participates in Hirschsprung's disease ( HSCR ). Here, we discovered that LPS increased in HSCR tissues. Furthermore, LPS treatment suppressed the proliferation and differentiation of neural precursor cells ( NPC s) or proliferation and migration of human 293T cells. ADAR 2 (adenosine deaminase acting on RNA 2)‐mediated post‐transcriptional adenosine‐to‐inosine RNA editing promotes cancer progression. We show that increased LPS activates ADAR 2 and subsequently regulates the A‐to‐I RNA editing which suppresses the miR‐142 expression. RNA sequencing combined with qRT ‐ PCR suggested that ADAR 2 restrain cell migration and proliferation via pri‐miR‐142 editing and STAU 1 up‐regulation. In conclusion, the findings illustrate that LPS participates in HSCR through the LPS ‐ ADAR 2‐miR‐142‐ STAU 1 axis.