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ORIGINAL RESEARCH article

Front. Pharmacol.
Sec. Pharmacology of Anti-Cancer Drugs
Volume 15 - 2024 | doi: 10.3389/fphar.2024.1470217

Targeting Autophagy: Polydatin's Role in Inducing Cell Death in AML

Provisionally accepted
Ping Fu Ping Fu 1Qing Luo Qing Luo 1Chao Wang Chao Wang 1Liping Chen Liping Chen 2Chang Dong Chang Dong 2Ke Yang Ke Yang 2Guang Wu Guang Wu 1*
  • 1 The Second Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, China
  • 2 COSAY (Guangzhou) Biotech Co., Ltd., Guangzhou, China

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

    Acute myeloid leukemia (AML), a malignant disorder of the hematopoietic system, arises from leukemic stem cells (LSCs) and is the most prevalent form of blood cancer in adults. This study aimed to evaluate the therapeutic potential of polydatin (PD) in AML through ex vivo and in vivo studies, respectively. This study was prompted by PD's novel role in enhancing tumor apoptosis and modulating autophagy. In vitro studies were conducted using the PD-responsive AML cell line KASUMI-1 and found that PD was able to suppress cell proliferation and induce apoptosis by regulating the autophagy pathway. Subsequently, molecular docking was employed to predict the interaction between PD and Autophagy-related protein 5 (ATG5), a key regulator in the autophagy pathway. It was observed that PD inhibited the ubiquitination of ATG5 and enhanced its protein stability, leading to an increase in ATG5 protein levels and subsequent activation of the autophagy pathway (see in Abstract Graphed). The effectiveness and safety of PD in treating AML were confirmed through in vivo experiments using a mouse transplant tumor model, yielding definitive results. Collectively, these results suggest that PD is a promising candidate for the early therapeutic intervention of AML, with a strong potential for clinical application.

    Keywords: Polydatin, AML, Atg5, Autophagy, proliferation, Apoptosis

    Received: 25 Jul 2024; Accepted: 23 Sep 2024.

    Copyright: © 2024 Fu, Luo, Wang, Chen, Dong, Yang and Wu. 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: Guang Wu, The Second Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, China

    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.