From monocyte‐derived macrophages to resident macrophages—how metabolism leads their way in cancer

单核细胞 巨噬细胞 细胞代谢 新陈代谢 癌症 癌细胞 生物 癌症研究 免疫学 微生物学 细胞生物学 生物化学 遗传学 体外
作者
Ummi Ammarah,Andreia Pereira‐Nunes,Marcello Delfini,Massimiliano Mazzone
出处
期刊:Molecular Oncology [Wiley]
标识
DOI:10.1002/1878-0261.13618
摘要

Macrophages are innate immune cells that play key roles during both homeostasis and disease. Depending on the microenvironmental cues sensed in different tissues, macrophages are known to acquire specific phenotypes and exhibit unique features that, ultimately, orchestrate tissue homeostasis, defense, and repair. Within the tumor microenvironment, macrophages are referred to as tumor‐associated macrophages (TAMs) and constitute a heterogeneous population. Like their tissue resident counterpart, TAMs are plastic and can switch function and phenotype according to the niche‐derived stimuli sensed. While changes in TAM phenotype are known to be accompanied by adaptive alterations in their cell metabolism, it is reported that metabolic reprogramming of macrophages can dictate their activation state and function. In line with these observations, recent research efforts have been focused on defining the metabolic traits of TAM subsets in different tumor malignancies and understanding their role in cancer progression and metastasis formation. This knowledge will pave the way to novel therapeutic strategies tailored to cancer subtype‐specific metabolic landscapes. This review outlines the metabolic characteristics of distinct TAM subsets and their implications in tumorigenesis across multiple cancer types.

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