The Role of miR-182-5p in Hepatocarcinogenesis of Trichloroethylene in Mice

The Role of miR-182-5p in Hepatocarcinogenesis of Trichloroethylene in Mice Trichloroethylene (TCE), commonly used as an industrial solvent, is ubiquitous in our living environment. TCE exposure can induce hepatocellular carcinoma (HCC) in mice, but the underlying mechanisms remain elusive. To understand the role of miRNA in the hepatocarcinogenesis of TCE, we examined the miRNA expression profiles by microarray in the liver of B6C3F1 male mice exposed to TCE at 0 or 1000 mg/kg b.w. Nine differentially expressed miRNAs were identified, out of which miR-182-5p exhibited the highest increase in expression. Moreover, the TCE-induced upregulation of miR182-5p in mouse liver was dose dependent and correlated with promoter DNA hypomethylation. Treatment of mouse liver cell lines (BNL CL.2 and Hepa1-6) with TCE at non-toxic doses (0.1 and/or 0.3 mM) significantly increased the expression level of miR-182-5p accompanied with elevated cell proliferation. The TCE-induced cell proliferation was further found to be mediated by miR-182-5p overexpression. Additionally, tumor suppressor gene Cited2, which was downregulated in TCE exposed mouse liver cells, was proved to be a direct target of miR-182-5p. In conclusion, TCE might up-regulate miR-182-5p expression by DNA hypomethylation, which could suppress Cited2 and improve cell proliferation rate, resulting in liver tumor. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Toxicological Sciences Oxford University Press

The Role of miR-182-5p in Hepatocarcinogenesis of Trichloroethylene in Mice

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Publisher
Oxford University Press
Copyright
© The Author 2016. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com
ISSN
1096-6080
eISSN
1096-0929
D.O.I.
10.1093/toxsci/kfw246
Publisher site
See Article on Publisher Site

Abstract

Trichloroethylene (TCE), commonly used as an industrial solvent, is ubiquitous in our living environment. TCE exposure can induce hepatocellular carcinoma (HCC) in mice, but the underlying mechanisms remain elusive. To understand the role of miRNA in the hepatocarcinogenesis of TCE, we examined the miRNA expression profiles by microarray in the liver of B6C3F1 male mice exposed to TCE at 0 or 1000 mg/kg b.w. Nine differentially expressed miRNAs were identified, out of which miR-182-5p exhibited the highest increase in expression. Moreover, the TCE-induced upregulation of miR182-5p in mouse liver was dose dependent and correlated with promoter DNA hypomethylation. Treatment of mouse liver cell lines (BNL CL.2 and Hepa1-6) with TCE at non-toxic doses (0.1 and/or 0.3 mM) significantly increased the expression level of miR-182-5p accompanied with elevated cell proliferation. The TCE-induced cell proliferation was further found to be mediated by miR-182-5p overexpression. Additionally, tumor suppressor gene Cited2, which was downregulated in TCE exposed mouse liver cells, was proved to be a direct target of miR-182-5p. In conclusion, TCE might up-regulate miR-182-5p expression by DNA hypomethylation, which could suppress Cited2 and improve cell proliferation rate, resulting in liver tumor.

Journal

Toxicological SciencesOxford University Press

Published: Mar 1, 2017

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