Kumar Sudhir, Mittal Sonam, Gupta Prachi, Singh Mona, Chaluvally-Raghavan Pradeep, Pradeep Sunila
Department of Obstetrics and Gynecology, Medical College of Wisconsin, Milwaukee, WI 53226, USA.
Department of Physiology, Medical College of Wisconsin, Milwaukee, WI 53226, USA.
Cancers (Basel). 2022 Oct 25;14(21):5224. doi: 10.3390/cancers14215224.
The interaction between tumor cells and macrophages in the tumor microenvironment plays an essential role in metabolic changes in macrophages and reprograms them towards a pro-tumorigenic phenotype. Increasing evidence indicates that macrophage metabolism is a highly complex process and may not be as simple as previously thought. Pro-inflammatory stimuli switch macrophages towards an M1-like phenotype and rely mainly on aerobic glycolysis and fatty acid synthesis, whereas anti-inflammatory stimuli switch macrophages towards an M2-like phenotype. M2-like macrophages depend more on oxidative phosphorylation (OXPHOS) and fatty acid oxidation. However, this metabolically reprogrammed phenotypic switch in macrophages remained a mystery for a while. Therefore, through this review, we tend to describe how macrophage immunometabolism determines macrophage phenotypes and functions in tumor microenvironments (TMEs). Furthermore, we have discussed how metabolic reprogramming in TAM can be used for therapeutic intervention and drug resistance in ovarian cancer.
肿瘤微环境中肿瘤细胞与巨噬细胞之间的相互作用在巨噬细胞的代谢变化中起着至关重要的作用，并将它们重编程为促肿瘤表型。越来越多的证据表明，巨噬细胞代谢是一个高度复杂的过程，可能不像以前认为的那么简单。促炎刺激使巨噬细胞向M1样表型转变，主要依赖有氧糖酵解和脂肪酸合成，而抗炎刺激使巨噬细胞向M2样表型转变。M2样巨噬细胞更多地依赖氧化磷酸化（OXPHOS）和脂肪酸氧化。然而，巨噬细胞这种代谢重编程的表型转换在一段时间内仍是个谜。因此，通过本综述，我们倾向于描述巨噬细胞免疫代谢如何决定肿瘤微环境（TME）中巨噬细胞的表型和功能。此外，我们还讨论了肿瘤相关巨噬细胞（TAM）中的代谢重编程如何用于卵巢癌的治疗干预和耐药性研究。
