p38/p53/miR-200a-3p feedback loop promotes oxidative stress-mediated liver cell death

Cell Cycle
Yongtao XiaoWei Cai

Abstract

Although our previous studies have provided evidence that oxidative stress has an essential role in total parenteral nutrition (TPN)-associated liver injury, the mechanisms involved are incompletely understood. Here, we show the existence of crosstalk between the miR-200 family of microRNAs and oxidative stress. The members of the miR-200 family are markedly enhanced in hepatic cells by hydrogen peroxide (H2O2) treatment. The upregulation of miR-200-3p in turn modulates the H2O2-mediated oxidative stress response by targeting p38α. The enhanced expression of miR-200-3p mimics p38α deficiency and promotes H2O2-induced cell death. Members of the miR-200 family that are known to inhibit the epithelial to mesenchymal transition (EMT) are induced by the tumor suppressor p53. Here, we show that p53 phosphorylation at Ser 33 contributes to H2O2-induced miR-200s transcription. In addition, we show that p38α can directly phosphorylate p53 at serine 33 upon H2O2 exposure. Thus, we suggest that in liver cells, the oxidative stress-induced, p38α-mediated phosphorylation of p53 at Ser33 is essential for the functional regulation of oxidative stress-induced miR-200 transcription by p53. Collectively, our data indicate that the p53-dependent ...Continue Reading

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Citations

Sep 21, 2016·Tumour Biology : the Journal of the International Society for Oncodevelopmental Biology and Medicine·Jun-Yu KeJian-Wei Jiang
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Methods Mentioned

BETA
ChIP
immunoprecipitation
PCR
transfection
Infection
fluorescence
flow cytometry
Luciferase
fluorescence assay
Assay

Software Mentioned

TALE Toolbox

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