Chaperone gp96 mediates ER-α36 cell membrane expression

Junwei Hou; Mengmeng Deng; Xin Li; Weiwei Liu; Xiaoyu Chu; Jing Wang; Feng Chen; Songdong Meng

doi:10.18632/oncotarget.5273

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

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:

Chaperone gp96 mediates ER-α36 cell membrane expression

Junwei Hou, Mengmeng Deng, Xin Li, Weiwei Liu, Xiaoyu Chu, Jing Wang, Feng Chen _ and Songdong Meng

PDF | HTML | How to cite

Oncotarget. 2015; 6:31857-31867. https://doi.org/10.18632/oncotarget.5273

Metrics: PDF 1662 views | HTML 2312 views | ?

Abstract

Junwei Hou1, Mengmeng Deng1, Xin Li1, Weiwei Liu1, Xiaoyu Chu1, Jing Wang2, Feng Chen2, Songdong Meng1

1CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences (CAS), Beijing 100101, P.R. China

2Shenogen Pharma Group, Changping District, Beijing 102206, P.R. China

Correspondence to:

Songdong Meng, e-mail: [email protected]

Feng Chen, e-mail: [email protected]

Keywords: ER-α36, gp96, ubiquitin, MAPK, breast cancer

Received: April 26, 2015 Accepted: August 28, 2015 Published: September 10, 2015

ABSTRACT

ER (estrogen receptor)-α36, a variant of human ERα, activates non-genomic cell signaling pathways. ER-α36 on the cell membrane plays a role in breast cancer growth and development, and contributes to tamoxifen resistance. However, it is not understood how cell membrane expression of ER-α36 is regulated. In this study, we investigated the role of cell membrane glycoprotein 96 (mgp96) in the regulation of ER-α36 expression and signaling. We found that the C-terminal domain of mgp96 directly interacts with ER-α36 on the cell membrane of breast tumor cells. This interaction stabilizes the ER-α36 protein, thereby increasing its signaling, which, in turn, increases tumor cell growth and invasion. Moreover, targeting mgp96 with siRNA or monoclonal antibody (mAb) blocks the mgp96-ER-α36 interaction and inhibits breast cancer growth and invasion both in vitro and in vivo. These results provide insights into the modulation of cell membrane ER-α36 expression and suggest that mgp96 could be a potential therapeutic target for ER-α36-overexpressing breast cancer.

All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 5273

Publication Alerts

Post-Publication Promotion

Research Papers:

Chaperone gp96 mediates ER-α36 cell membrane expression

Abstract