CD36 介导的脂质重编程在肿瘤生态系统代谢适应中的作用

Tumour progression is increasingly recognised as a dynamic, complex ecosystem-driven metabolic plasticity and resource utilisation within the tumour microenvironment. Among metabolic regulators, CD36, an important mediator of lipid uptake, has an emerging role in the lipid-driven metabolic adaptation of cancer. CD36 facilitates the acquisition and use of exogenous fatty acids, enabling tumour cells to maintain bioenergetic homeostasis and growth. This metabolic rewiring supports tumour progression by establishing a complex metabolic symbiosis among heterogeneous cellular populations. CD36 has a significant role in determining the fate of various cancer-associated cells including fibroblasts, adipocytes and immune cells.

These tissue-driven, cell type- and environment-dependent lipid metabolic shifts allow the developing tumour to bypass metabolic stress and nutrient deprivation. While CD36-mediated alterations act as a crucial survival promoter for the 'winners' (tumour cells and immunosuppressive myeloid-derived suppressor cells or regulatory T cells), they simultaneously trigger exhaustion, lipid peroxidation and ferroptosis in the 'losers' (cytotoxic T cells and natural killer cells).

Consequently, CD36 functions as an essential metabolic 'emergency exit', allowing the tumour to escape starvation and survive despite recent therapies. This review synthesises current knowledge on CD36 as a metabolic bridge linking lipid uptake, metabolic symbiosis and tumour immune ecosystem remodelling.

We discuss how CD36-driven lipid metabolism integrates cellular crosstalk, nutrient competition to sustain progression in different cancers. Understanding the role of CD36 in tumour and immunometabolism in the tissue microenvironment highlights the importance of CD36 as a potential target through metabolic adaptations in shaping tumour evolution and clinical outcomes.