Nuclear factor erythroid-2-related factor regulates LRWD1 expression and cellular adaptation to oxidative stress in human embryonal carcinoma cells

doi:10.1016/j.biochi.2018.03.001

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Title:	Nuclear factor erythroid-2-related factor regulates LRWD1 expression and cellular adaptation to oxidative stress in human embryonal carcinoma cells
Authors:	Hung, Jui-Hsiang Wee, Shi-Kae Omar, Hany A. Su, Chia-Hui Chen, Hsing-Yi Chen, Pin-Shern Chiu, Chien-Chih Wu, Ming-Syuan Teng, Yen-Ni
Contributors:	Chia Nan Univ Pharm & Sci, Dept Biotechnol Chia Nan Univ Pharm & Sci, Drug Discovery & Dev Ctr Natl Univ Tainan, Dept Biol Sci & Technol Univ Sharjah, Sharjah Inst Med Res Univ Sharjah, Coll Pharm Beni Suef Univ, Fac Pharm, Dept Pharmacol Kaohsiung Med Univ, Dept Biotechnol
Keywords:	LRWD1 Nrf2 Oxidative stress Reactive oxygen species Transcriptional regulation
Date:	2018-05
Issue Date:	2019-11-15 15:44:09 (UTC+8)
Publisher:	ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
Abstract:	Leucine-rich repeats and WD repeat domain-containing protein 1 (LRWD1) is implicated in the regulation of signal transduction, transcription, RNA processing and tumor development. However, LRWD1 transcriptional regulation is not fully understood. This study aimed to investigate the relationship between LRWD1 expression and reactive oxygen species (ROS) level in human embryonal carcinoma cell line, NT2/D1 cells, which will help in understanding the transcriptional regulatory role of ROS in cells. Results showed that the exposure of NT2/D1 cells to various concentrations of hydrogen peroxide (H2O2) and the nitric oxide (NO) donor sodium nitroprusside (SNP) caused a significant increase in the mRNA and protein expression of LRWD1. In addition, LRWD1 promoter luciferase reporter assay, and Chromatin Immunoprecipitation assay (CHIP assay) showed that nuclear factor erythroid-2-related factor (Nrf2) was involved in the regulation of LRWD1 expression in response to oxidative stress. The involvement of Nrf2 was confirmed by shRNA-mediated knockdown of Nrf2 in NT2/D1 cells, which caused a significant decrease in LRWD1 expression in response to oxidative stress. Similarly, LRWD1 knockdown resulted in the accumulation of H2O2 and superoxide anion radical (O2-). Blocking ROS production by N-acetyl cysteine (NAC) protected NT2/D1 shLRWD1cells from H2O2-induced cell death. Collectively, oxidative stress increased LRWD1 expression through a Nrf2-dependent mechanism, which plays an important role in cellular adaptation to oxidative stress. These results highlight an evidence, on the molecular level, about LRWD1 transcriptional regulation under oxidative stress. (C) 2018 Elsevier B.V. and Societe Francaise de Biochimie et Biologie Moleculaire (SFBBM). All rights reserved.
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Relation:	Journal of Aerosol Science, v.148, pp.99-106
Appears in Collections:	[Dept. of Life and Health Science] Periodical Articles

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