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

Yao Xu1, Ying Luo1, Zhen-Yu Wang1

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

Oncotarget
|December 31, 2016
PubMed

Insights

The study reveals that MRTF-A overexpression enhances cancer cell resistance to doxorubicin chemotherapy by boosting Nrf2 expression. Knocking down MRTF-A or Nrf2 reverses this resistance, uncovering a new chemotherapy resistance pathway.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Chemotherapeutic drug resistance is a major challenge in cancer therapy.
  • Myocardin-related transcription factor A (MRTF-A) promotes tumor invasion and metastasis.
  • The role of MRTF-A in chemotherapy resistance is largely unexplored.

Purpose of the Study:

  • To investigate the role of MRTF-A in doxorubicin resistance in cancer cells.
  • To elucidate the molecular mechanisms underlying MRTF-A-mediated chemoresistance.

Main Methods:

  • MRTF-A and Nrf2 expression levels were manipulated (overexpression and knockdown).
  • Doxorubicin-induced apoptosis was assessed in cancer cells.
  • The interaction between MRTF-A, SRF, and the Nrf2 promoter was analyzed.

Main Results:

  • MRTF-A overexpression conferred resistance to doxorubicin by increasing Nrf2 expression.
  • Knockdown of MRTF-A or Nrf2 reversed doxorubicin resistance.
  • MRTF-A regulates Nrf2 transcription via a complex with SRF binding to the Nrf2 promoter's CarG box.

Conclusions:

  • MRTF-A plays a significant role in doxorubicin resistance.
  • A novel resistance pathway involving MRTF-A, SRF, and Nrf2 in doxorubicin chemotherapy was identified.
Keywords:
MRTF-ANrf2drug resistancehela

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