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Caveolae and Signalling in Cancer

Authors: Ubaldo E. Martinez-Outschoorn, Maria Peiris-Pagés, Richard G. Pestell, Federica Sotgia, Michael P. Lisanti

Published in: Nature Reviews Cancer, April 2015

DOI: 10.1038/nrc3915

PMID: 25855493

Abstract

This review article explores the role of caveolae—small, flask-shaped invaginations in the plasma membrane—and their principal structural protein, caveolin-1 (CAV1), in cancer biology. It discusses how caveolae and CAV1 influence various cellular processes, including signal transduction, lipid regulation, and endocytosis, and how these functions contribute to tumor development, progression, and metastasis.

Key Points

  • Signal Transduction: Caveolae serve as platforms for organizing and regulating signaling molecules, affecting pathways such as MAPK/ERK and PI3K/AKT, which are critical in cancer cell proliferation and survival.
  • Lipid Regulation: Caveolae are involved in lipid homeostasis, influencing membrane composition and the localization of signaling molecules.
  • Endocytosis and Transcytosis: Caveolae-mediated endocytosis affects the internalization of various molecules, impacting nutrient uptake and signal transduction in cancer cells.
  • Role of Caveolin-1: CAV1 has a dual role in cancer, acting as a tumor suppressor in early stages and as a promoter of tumor progression and metastasis in advanced stages.
  • Therapeutic Implications: Targeting caveolae and CAV1-related pathways presents potential strategies for cancer therapy, including disrupting caveolae-mediated signaling and modulating CAV1 expression.

Conclusion

The review highlights the multifaceted roles of caveolae and CAV1 in cancer, emphasizing their contributions to tumor biology and their potential as targets for therapeutic intervention. Understanding the context-dependent functions of CAV1 is crucial for developing effective cancer treatments.

Conflict of Interest: The authors declare no competing interests.

Funding: Not specified in the article.

Access Full Article

You can read the full publication via PubMed Central: https://pubmed.ncbi.nlm.nih.gov/25801618/

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