SET mediates TCE-induced liver cell apoptosis through dephosphorylation and upregulation of nucleolin

Xiaohu Ren; Xinfeng Huang; Xifei Yang; Yungang Liu; Wei Liu; Haiyan Huang; Desheng Wu; Fei Zou; Jianjun Liu

doi:10.18632/oncotarget.16785

Oncotarget

Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

Its scope is unique. The term "oncotarget" encompasses all molecules, pathways, cellular functions, cell types, and even tissues that can be viewed as targets relevant to cancer as well as other diseases. The term was introduced in the inaugural Editorial, Introducing Oncotarget.

As of January 1, 2022, Oncotarget has shifted to a continuous publishing model. Papers will now be published continuously within yearly volumes in their final and complete form and then quickly released to Pubmed.

Subscribe to receive alerts once a paper has been published by Oncotarget.

Learn about our FREE

Post-Publication Promotion Services

50% on all publication fees until the end of 2024.

Impact Journals, LLC is the publisher of Oncotarget: www.impactjournals.com.

Impact Journals is a member of the Wellcome Trust List of Compliant Publishers.

Impact Journals is a member of the Society for Scholarly Publishing.

On December 23, 2022, Oncotarget server experienced a DDoS attack. As a result, Oncotarget site was inaccessible for a few hours. Oncotarget team swiftly dealt with the situation and took it under control. This malicious action will be reported to the FBI.

Research Papers:

SET mediates TCE-induced liver cell apoptosis through dephosphorylation and upregulation of nucleolin

Xiaohu Ren, Xinfeng Huang, Xifei Yang, Yungang Liu, Wei Liu, Haiyan Huang, Desheng Wu, Fei Zou and Jianjun Liu _

PDF | HTML | Supplementary Files | How to cite

Oncotarget. 2017; 8:40958-40966. https://doi.org/10.18632/oncotarget.16785

Metrics: PDF 1479 views | HTML 2361 views | ?

Abstract

Xiaohu Ren1,2, Xinfeng Huang1, Xifei Yang1, Yungang Liu2, Wei Liu1, Haiyan Huang1, Desheng Wu1, Fei Zou2 and Jianjun Liu1

1Key Laboratory of Modern Toxicology of Shenzhen, Shenzhen Center for Disease Control and Prevention, Shenzhen, 518055, China

2School of Public Health, Southern Medical University, Guangzhou, 510515, China

Correspondence to:

Jianjun Liu, email: [email protected], [email protected]

Fei Zou, email: [email protected]

Keywords: trichloroethylene, nucleolin, SET, hepatic cytotoxicity, proteomics

Received: August 26, 2016 Accepted: February 12, 2017 Published: April 03, 2017

ABSTRACT

Trichloroethylene (TCE) is an occupational and environmental chemical that can cause severe hepatotoxicity. While our previous studies showed that the phosphatase inhibitor SET is a key mediator of TCE-induced liver cell apoptosis, the molecular mechanisms remain elusive. Using quantitative phosphoproteomic analysis, we report here that nucleolin is a SET-regulated phosphoprotein in human liver HL-7702 cells. Functional analysis suggested that SET promoted dephosphorylation of nucleolin, decreased its binding to its transcriptional activator, c-myc, and upregulated nucleolin expression in TCE-treated cells. Importantly, TCE-induced hepatocyte apoptosis was significantly attenuated when nucleolin was downregulated with specific siRNAs. These findings indicate that TCE may induce hepatocyte apoptosis via SET-mediated dephosphorylation and overexpression of nucleolin.

All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 16785

Publication Alerts

Post-Publication Promotion

Publication Discount

Research Papers:

SET mediates TCE-induced liver cell apoptosis through dephosphorylation and upregulation of nucleolin

Abstract