MINI REVIEW article
Front. Immunol.
Sec. Cancer Immunity and Immunotherapy
This article is part of the Research TopicT Cell Exhaustion in Chronic Infection and CancerView all 6 articles
Lipid Metabolic Reprogramming in the Tumor Microenvironment and Its Mechanistic Role in Immunosuppressive Cells
Provisionally accepted- 1Department of Surgical Oncology and General Surgery, The First Hospital of China Medical University, Shenyang, Liaoning 110001, China., Shenyang, China
- 2Department of Thoracic Surgery, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China
- 3Department of E.N.T., Shengjing Hospital of China Medical University, Shenyang, 110003, PR China.Address: No. 36 Sanhao Street, Shenyang 110004, Liaoning Province, China., shenyang, China
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Introduction "Cold tumors" are malignancies with poor immune infiltration and limited response to immunotherapy, largely shaped by an immunosuppressive tumor microenvironment (TME)1-3. Lipid metabolic reprogramming has emerged as a central mechanism sustaining this suppression. Rapidly proliferating tumor cells deplete nutrients and release byproducts, generating hypoxia, acidosis, and scarcity, which force both tumor and immune cells to rewire their metabolism4,5.Under these stresses, not only tumor cells but also immune cells undergo "immunometabolic" reprogramming to adapt to the hostile environment6,7. Lipids serve as fuels, signaling mediators, and membrane components, and their altered metabolism profoundly affects immune regulation8,9. This mini review highlights how lipid reprogramming supports key immunosuppressive populations in the TME— regulatory T cells (Tregs), tumor-associated macrophages (TAMs), and myeloid-derived suppressor cells (MDSCs)—and explores therapeutic strategies that target lipid metabolism to improve cancer immunotherapy.
Keywords: Lipid metabolic, metabolic reprogramming, immunometabolic, regulatory T cells, Tumor-associated macrophages, myeloid-derived suppressor cells
Received: 19 Oct 2025; Accepted: 29 Oct 2025.
Copyright: © 2025 Liu, Wang, Li, Li, Shi, Xu and Wang. 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:
Yan Xu, yanxu@cmu.edu.cn
Jin Wang, wangj10@sj-hospital.org
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.
