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Updated: May 6, 2026

Tractable In Vivo Reprogramming of Tumor Cells to Type 1 Conventional Dendritic Cell-like Cells
Published on: August 1, 2025
Targeting caveolin-1: dual challenges in tumor immunity and drug therapy strategies
Xiyue Ge1, Tianyi Song1, Xiangyan Guo1
1Laboratory of Stem Cell Regulation with Chinese Medicine and Its Application, School of Pharmacy, Hunan University of Chinese Medicine, Changsha, 410208, Hunan, China.
Abstract:
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.
Insights
Caveolin-1 (Cav-1) influences tumor immunity by altering lipid metabolism and promoting immune evasion. Targeting Cav-1 offers potential for novel cancer therapies, but its complex roles require further study.
Area of Science:
- Oncology
- Immunology
- Molecular Biology
Background:
- Tumor immunity is vital for suppressing cancer initiation and progression.
- Tumor metabolic reprogramming and immune evasion are key factors in cancer development.
- Caveolin-1 (Cav-1) is implicated in cell signaling, lipid metabolism, and immune responses, and is often upregulated in various cancers.
Purpose of the Study:
- To review the structure and functions of Cav-1, focusing on its role in tumor-associated immune cells.
- To discuss how Cav-1-mediated lipid metabolic reprogramming impacts antitumor immunity.
- To highlight challenges in developing Cav-1-targeting drugs and its potential as a therapeutic target.
Main Methods:
- Literature review focusing on Cav-1's role in tumor immunity and metabolism.
- Analysis of Cav-1 expression patterns across different cancer subtypes.
- Synthesis of current understanding of Cav-1's mechanisms in immune evasion and therapy resistance.
Main Results:
- Cav-1 is frequently upregulated in many cancers but shows context-dependent expression, varying by cancer subtype.
- Cav-1 mediates lipid metabolic reprogramming, which can regulate antitumor immunity.
- Tumor metabolic reprogramming, influenced by Cav-1, can drive immunosuppression through cytokines like TGF-β and IL-4, leading to immune evasion.
Conclusions:
- Cav-1 is a potential biomarker and therapeutic target for cancer due to its role in tumor immunity and metabolism.
- The heterogeneous expression and context-specific functions of Cav-1 present challenges for drug development.
- Further research into Cav-1's mechanisms in tumor immunity is crucial for developing effective cancer therapies.
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