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BRIEF RESEARCH REPORT article

Front. Cell Death
Sec. Non-Apoptotic Regulated Cell Death
Volume 3 - 2024 | doi: 10.3389/fceld.2024.1507960

ATF4-mediated expression of NOXA is critical for Necroptosis driven by Glucose Deprivation

Provisionally accepted
Swati Choksi Swati Choksi 1*Sasiprapa Sonkaew Sasiprapa Sonkaew 2Ruwaida Rajna Ruwaida Rajna 1Jiong Yan Jiong Yan 1Zhaoshan Liu Zhaoshan Liu 1Siriporn Jitkaew Siriporn Jitkaew 2Zhenggang Liu Zhenggang Liu 1*
  • 1 National Institutes of Health (NIH), Bethesda, United States
  • 2 Chulalongkorn University, Bangkok, Bangkok, Thailand

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

    Glucose deprivation (GD), a common metabolic stress condition, has been recognized as a potent inducer of necroptotic cell death. Our previous findings suggested that the mitochondrial protein, Noxa, may be involved in mediating the release of mitochondrial DNA during GD-induced ZBP1-dependent necroptotic pathway. However, the functional significance of Noxa in necroptosis under GD treatment remains unclear. Here, we investigated the role of Noxa in GD-induced necroptosis and the underlying molecular mechanisms governing its expression. We revealed that Noxa is required for the induction of necroptosis under GD. We also demonstrated that the upregulation of Noxa induced by GD is mediated by ATF4, a key transcription factor. These results provide insights into the regulatory mechanisms underlying Noxa dynamics during GD treatment and highlights its potential as a therapeutic target in cancer therapy and necroptosis-related diseases.

    Keywords: glucose deprivation, Noxa, ATF4, necroptosis, Cell Death

    Received: 08 Oct 2024; Accepted: 17 Dec 2024.

    Copyright: © 2024 Choksi, Sonkaew, Rajna, Yan, Liu, Jitkaew and Liu. 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:
    Swati Choksi, National Institutes of Health (NIH), Bethesda, United States
    Zhenggang Liu, National Institutes of Health (NIH), Bethesda, United States

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