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REVIEW article

Front. Cell Dev. Biol.
Sec. Cell Death and Survival
Volume 12 - 2024 | doi: 10.3389/fcell.2024.1500880
This article is part of the Research Topic Survival Strategies: Cellular Responses to Stress and Damage View all 4 articles

HSF1 at the crossroads of chemoresistance: From current insights to future horizons in cell death mechanisms

Provisionally accepted
Shruti Ghai Shruti Ghai Rejina Shrestha Rejina Shrestha Kuo-Hui Su Kuo-Hui Su *
  • Department of Cell and Cancer Biology, College of Medicine and Life Sciences, The University of Toledo, Toledo, OH, United States

The final, formatted version of the article will be published soon.

    Heat Shock Factor 1 (HSF1) is a major transcriptional factor regulating the heat shock response and has become a potential target for overcoming cancer chemoresistance. This review comprehensively examines HSF1’s role in chemoresistance and its potential as a therapeutic target in cancer. We explore the complex, intricate mechanism that regulates the activation of HSF1, HSF1’s function in promoting resistance to chemotherapy, and the strategies used to manipulate HSF1 for therapeutic benefit. In addition, we discuss emerging research implicating HSF1’s roles in autophagy, apoptosis, DNA damage repair, drug efflux, and thus chemoresistance. This article highlights the significance of HSF1 in cancer chemoresistance and its potential as a target for enhancing cancer treatment efficacy.

    Keywords: heat shock factor 1, chemoresistance, proteotoxic stress response, Autophagy, Apoptosis, drug efflux

    Received: 24 Sep 2024; Accepted: 18 Dec 2024.

    Copyright: © 2024 Ghai, Shrestha and Su. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence: Kuo-Hui Su, Department of Cell and Cancer Biology, College of Medicine and Life Sciences, The University of Toledo, Toledo, OH, United States

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.