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REVIEW article

Front. Oncol.
Sec. Cancer Immunity and Immunotherapy
Volume 14 - 2024 | doi: 10.3389/fonc.2024.1449696

Interactions between Tumor-Associated Macrophages and Regulated Cell Death: Therapeutic Implications in Immuno-Oncology

Provisionally accepted
  • 1 Department of Hepatopancreatobiliary Surgery, Second Affiliated Hospital of Harbin Medical University, Harbin, Jilin Province, China
  • 2 Department of Breast Surgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, China
  • 3 Huzhou Key Laboratory of Translational Medicine, Department of Hepatopancreatobiliary Surgery, The First People's Hospital of Huzhou, Huzhou, China
  • 4 Key Laboratory of Clinical Laboratory Diagnosis and Translational Research of Zhejiang Province, First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang Province, China
  • 5 National Center for International Research of Biological Targeting Diagnosis and Therapy, Guangxi Medical University, Nanning, Guangxi Zhuang Region, China
  • 6 Fujian Provincial Key Laboratory of Cancer Biotherapy, Fujian Provincial Cancer Hospital, Fuzhou, Fujian Province, China
  • 7 Fujian Provincial Key Laboratory of Translational Cancer Medicine, Fujian Provincial Cancer Hospital, Fuzhou, Fujian Province, China
  • 8 Department of Pathology, School of Clinical Medicine, LKS Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong, SAR China

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

    Tumor-associated macrophages (TAMs) play a pivotal role in sculpting the tumor microenvironment and influencing cancer progression, particularly through their interactions with various forms of regulated cell death (RCD), including apoptosis, pyroptosis, ferroptosis, and necroptosis. This review examines the interplay between TAMs and these RCD pathways, exploring the mechanisms through which they interact to promote tumor growth and advancement. We examine the underlying mechanisms of these intricate interactions, emphasizing their importance in cancer progression and treatment. Moreover, we present potential therapeutic strategies for targeting TAMs and manipulating RCD to enhance anti-tumor responses. These include approaches for reprogramming, recruiting, and eliminating TAMs to enhance their anti-tumor functions, as well as adjusting RCD pathways to amplify immune responses. These insights offer a novel perspective on tumor biology and provide a foundation for the development of more efficacious cancer therapies.

    Keywords: Tumor-associated macrophages, programmed cell death, Tumor Microenvironment, ferroptosis, pyroptosis, necroptosis, Apoptosis, cancer therapy

    Received: 15 Jun 2024; Accepted: 21 Oct 2024.

    Copyright: © 2024 Ge, Jiang, Yang, Dong, Tang, Xu and Zhong. 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:
    Chengwu Tang, Huzhou Key Laboratory of Translational Medicine, Department of Hepatopancreatobiliary Surgery, The First People's Hospital of Huzhou, Huzhou, China
    Yi Xu, Department of Hepatopancreatobiliary Surgery, Second Affiliated Hospital of Harbin Medical University, Harbin, 150001, Jilin Province, China
    Xiangyu Zhong, Department of Hepatopancreatobiliary Surgery, Second Affiliated Hospital of Harbin Medical University, Harbin, 150001, Jilin Province, 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.