Lipid metabolism plays a crucial role in tumor biology by influencing cancer progression and therapeutic resistance through intricate signaling networks and metabolic reprogramming.
Tumor cells manipulate fatty acids, cholesterol, and lipid droplets to promote growth, metastasis, and evade immune surveillance in the tumor microenvironment.
Cholesterol metabolism alterations, including lipid droplet accumulation, impact oncogenic pathways, membrane biosynthesis, and tumor aggressiveness.
Lipid droplets are actively regulated organelles influencing lipid homeostasis and impacting cancer cell survival under adverse conditions by generating reactive oxygen species.
Lipid metabolism extends its influence into the tumor immune microenvironment, hindering antitumor immune responses and fostering immunosuppression through nutrient competition and oxidative stress.
Metabolic adaptations in immune cells within the tumor niche, such as regulatory T cells and dendritic cells, affect their function and responses, highlighting the impact of lipid metabolism on immunosuppression.
Targeting lipid metabolic pathways in immune cells, such as dendritic cells and myeloid-derived suppressor cells, shows promise in reactivating antitumor immunity and delaying tumor progression.
Biomarkers associated with lipid metabolism, like FASN and FATP, are emerging as valuable tools for cancer diagnostics, prognostics, and guiding therapeutic strategies.
Modulating lipid metabolism for early cancer screening and integrating lipid-targeted strategies into immunotherapy presents a forward-looking approach in cancer management.
Inhibitors of lipid uptake molecules and lipid-based drug delivery systems hold potential in reducing immunosuppression and enhancing the efficacy of chemotherapeutic and immunomodulatory agents.
Understanding how lipid metabolism reprogramming influences tumorigenesis and immune regulation opens new avenues for personalized oncology approaches, combining metabolic modulation and immune activation for improved patient outcomes.