Targeting metabolic-epigenetic-immune axis in cancer: molecular mechanisms and therapeutic implications

Cancer cells orchestrate a highly dynamic and interconnected network spanning metabolic, epigenetic, and immune mechanisms to drive adaptive plasticity and continuous development. This review synthesizes emerging insights into the coevolutionary strategies employed by malignant and stromal cells-particularly tumor cells and immune populations-across the continuum of tumorigenesis, metastasis, and treatment resistance. During tumor initiation, cancer cells rewire metabolism and generate oncometabolites that reshape the chromatin architecture to support immune evasion. Concurrently, metabolic competition in the tumor microenvironment (TME) induces epigenetic exhaustion of cytotoxic T cells, whereas tumor-associated myeloid cells adopt immunosuppressive and angiogenic phenotypes via metabolite-dependent histone modifications to promote carcinogenesis. At metastatic frontiers, under the local metabolic pressure of target organs, tumor cells undergo epigenetic reprogramming to evade immune attacks and support colonization. Premetastatic niches are preconditioned through exosome-mediated transfer of metabolic enzymes and noncoding RNAs that reprogram resident cells before tumor cells arrive. In cancer immunotherapy, tumors often exploit metabolic adaptative strategies to inhibit cell death signaling pathways or the compensatory activation of self-protective mechanisms to circumvent immune-mediated cytotoxicity and develop resistance to immunotherapy. By mapping these dynamic interactions, we propose a novel conceptual framework of the "metabolic-epigenetic-immune axis" that transcends traditional compartmentalized approaches and helps to identify nodal convergence points for therapeutic co-targeting. This review also prioritizes multitarget inhibitors arising from the convergence of metabolic reprogramming, epigenetic plasticity, and immune evasion networks. An integrated approach to these pathways advances next-generation precision oncology strategies aimed at circumventing the evolutionary resilience of cancer.

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Publication Details

Journal
Signal Transduction and Targeted Therapy
Published
2026-01-26
DOI
https://doi.org/10.1038/s41392-025-02334-4
Citations
3
Primary Topic
Immune cells in cancer
Type
article
Field-Weighted Citation Impact
73.30

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article

Targeting metabolic-epigenetic-immune axis in cancer: molecular mechanisms and therapeutic implications

Xiyuan Luo, Yupei Zhao, Ming Cui, Lei You et al.
3 citations
Signal Transduction and Targeted Therapy
Immune cells in cancer
73.30
article

Targeting metabolic-epigenetic-immune axis in cancer: molecular mechanisms and therapeutic implications

Xiyuan Luo, Yupei Zhao, Ming Cui, Lei You, Feihan Zhou, Jialu Bai, Ruiling Xiao, Decheng Jiang, Xing Wang, Xiaohong Liu
article en
3 citations

Abstract

Cancer cells orchestrate a highly dynamic and interconnected network spanning metabolic, epigenetic, and immune mechanisms to drive adaptive plasticity and continuous development. This review synthesizes emerging insights into the coevolutionary strategies employed by malignant and stromal cells-particularly tumor cells and immune populations-across the continuum of tumorigenesis, metastasis, and treatment resistance. During tumor initiation, cancer cells rewire metabolism and generate oncometabolites that reshape the chromatin architecture to support immune evasion. Concurrently, metabolic competition in the tumor microenvironment (TME) induces epigenetic exhaustion of cytotoxic T cells, whereas tumor-associated myeloid cells adopt immunosuppressive and angiogenic phenotypes via metabolite-dependent histone modifications to promote carcinogenesis. At metastatic frontiers, under the local metabolic pressure of target organs, tumor cells undergo epigenetic reprogramming to evade immune attacks and support colonization. Premetastatic niches are preconditioned through exosome-mediated transfer of metabolic enzymes and noncoding RNAs that reprogram resident cells before tumor cells arrive. In cancer immunotherapy, tumors often exploit metabolic adaptative strategies to inhibit cell death signaling pathways or the compensatory activation of self-protective mechanisms to circumvent immune-mediated cytotoxicity and develop resistance to immunotherapy. By mapping these dynamic interactions, we propose a novel conceptual framework of the "metabolic-epigenetic-immune axis" that transcends traditional compartmentalized approaches and helps to identify nodal convergence points for therapeutic co-targeting. This review also prioritizes multitarget inhibitors arising from the convergence of metabolic reprogramming, epigenetic plasticity, and immune evasion networks. An integrated approach to these pathways advances next-generation precision oncology strategies aimed at circumventing the evolutionary resilience of cancer.

Signal Transduction and Targeted TherapyVol. 11(1)
Chinese Academy of Medical Sciences & Peking Union Medical College (CN), Peking Union Medical College Hospital (CN)
National Natural Science Foundation of China, Chinese Academy of Medical Sciences, Peking Union Medical College Hospital
Openalex Percentile: Top 0%
Immune cells in cancer
73.30
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