Tumor immunity is a crucial defense mechanism that suppresses tumor initiation and delays tumor progression. The interplay between tumor metabolic reprogramming and immune evasion is a putative determinant in the tumor progression. Caveolin-1 (Cav-1) is a major biomarker of caveolae and is involved in cell signaling, lipid metabolic reprogramming, and antitumor immune responses. Cav-1 is widely expressed in immune cells and tumor cells, with frequent upregulation in breast cancer, liver cancer, lung cancer, pancreatic cancer, glioma, and melanoma. However, Cav-1 expression is context-dependent and varies across cancer subtypes, including gastric cancer. This review discusses the structure and functions of Cav-1, emphasizing its role in tumor-associated immune cells. We summarized Cav-1-mediated lipid metabolic reprogramming regulates antitumor immunity and highlighted challenges in developing Cav-1-targeting drugs. Notably, tumor cell metabolic reprogramming not only supports cancer cell progression but also drives immunosuppression via inhibitory cytokines like transforming growth factor-β (TGF-β) and interleukin-4 (IL-4), fostering immune evasion and therapy resistance. While Cav-1 represents a potential biomarker and therapeutic target, its heterogeneous expression and context-specific functions necessitate further research to develop precise therapies. Future investigations into the mechanisms of Cav-1 in tumor immunity may pave the way for more effective cancer treatments.
Ge et al. (Mon,) studied this question.
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