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

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

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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: zhangtongcun@wust.edu.cn

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

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


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.

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