MRTF-A can activate Nrf2 to increase the resistance to doxorubicin

Yao Xu; Ying Luo; Zhen-yu Wang; Xi Li; Peng Zheng; Tong-cun Zhang

doi:10.18632/oncotarget.14246

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.

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:

MRTF-A can activate Nrf2 to increase the resistance to doxorubicin

Yao Xu _, Ying Luo, Zhen-yu Wang, Xi Li, Peng Zheng and Tong-cun Zhang

PDF | HTML | Supplementary Files | How to cite

Oncotarget. 2017; 8:8436-8446. https://doi.org/10.18632/oncotarget.14246

Metrics: PDF 1549 views | HTML 1869 views | ?

Abstract

Yao Xu1,*, Ying Luo1,*, Zhen-yu Wang1, Xi Li1, Peng Zheng1, Tong-cun Zhang1,2

1Institute of Biology and Medicine, Wuhan University of Science and Technology, Wuhan, 430065, China

2Key Laboratory of Industrial Microbiology, Ministry of Education and Tianjin City, College of Biotechnology, Tianjin University of Science and Technology, Tianjin, 300457, China

*These authors have contributed equally to this work

Correspondence to:

Tong-cun Zhang, email: [email protected]

Keywords: MRTF-A, Nrf2, hela, drug resistance

Received: June 21, 2016 Accepted: December 01, 2016 Published: December 27, 2016

ABSTRACT

Chemotherapeutic drugs resistance was considered to be the major obstacle for cancer therapy. MRTF-A, co-activators of serum response factor (SRF), promoted tumor cell invasion and metastasis in cancer. So far there has been no relevant reports about MRTF-A’ role in tumor chemotherapy. Here, we reported that MRTF-A overexpression conferred resistance to doxorubicin mediated apoptosis by significantly increasing the expression of Nrf2 which was an important molecule associated with the resistance of anticancer drugs. If MRTF-A was knocked down, could the corresponding results be obtained? Moreover, we showed that overexpression MRTF-A had no remarkable effect to doxorubicin mediated apoptosis in cancer cells when knocking down Nrf2. Further studies showed that MRTF-A regulated the transcriptional activity of Nrf2 by forming a complex with SRF binding to the CarG box which existed on Nrf2 promoter region. On the whole, our study revealed a novel possible resistant pathway to doxorubicin.

All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 14246

Publication Alerts

Research Papers:

MRTF-A can activate Nrf2 to increase the resistance to doxorubicin

Abstract