생화학분자생물학회

	Name: Do Sik Min ( minds@yonsei.ac.kr )
	2019-present	Professor, College of Pharmacy, Yonsei University
	2004-2019	Associate Professor, Department of Molecular biology, Pusan National University
	2009-2010	Visiting Associate Project Scientist, College of Medicine, University of California, San Diego
	1999-2004	Instructor and Assistant professor, Department of Physiology, College of Medicine, The Catholic University of Korea
	1998-1999	Research Professor, Department of Biochemistry, College of Medicine, Chungbuk National University
	1996-1998	Post-doctor, Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine,
	1993-1996	Ph.D., Department of Life Science, Pohang University of Science and Technology (POSTECH),
	1991-1993	MS, Department of Life Science, Pohang University of Science and Technology (POSTECH),
	1987-1989	MS, Department of Biotechnology, Yonsei University
	1983-1987	BS, Department of Biotechnology, Yonsei University

Metabolic crosstalk among cancer-associated fibroblasts, adipocytes and immune cells as an immunosuppressive tumor microenvironment driver

The tumor microenvironment (TME) is a complex ecosystem composed of not only malignant cells but also diverse stromal and immune cell populations that collectively shape tumor behavior. Metabolism is a central regulator of the TME, orchestrating intercellular communication through altered nutrients and signaling pathways to influence both the metabolic plasticity of cancer cells and functional balance of immune populations, ultimately determining tumor progression and antitumor immunity. Although tumor-intrinsic metabolic programs have been extensively characterized, emerging evidence highlights stromal metabolism as the dominant force sculpting immune responses within the TME. Among the nonmalignant stromal constituents, cancer-associated fibroblasts and cancer-associated adipocytes have emerged as metabolically active hubs that release and redistribute key metabolites, such as lactate, fatty acids and amino acids, to modulate the activity of both tumor and immune cells. Here we integrate recent advances in the understanding of stromal-immune metabolic crosstalk and elucidates how diverse metabolic mechanisms, including nutrient competition, mitochondrial remodeling, redox imbalance and immunometabolic rewiring, collectively reinforce an immunosuppressive TME and drive therapeutic resistance. Our study highlights the emerging strategies for selectively reprogramming these metabolic networks as potential therapeutic avenues. Deciphering these multilayered interactions will establish a conceptual and mechanistic foundation for reprogramming TME, restoring immune competence and enhancing the efficacy of current immunotherapies through metabolism-targeted interventions.


Exp Mol Med. 2026 Feb 13. doi: 10.1038/s12276-026-01650-1
https://pubmed.ncbi.nlm.nih.gov/41688740/