Abstract
Caveolin-1 (CAV1) is an oncogenic membrane protein associated with endocytosis, extracellular matrix organisation, cholesterol distribution, cell migration and signaling. Recent studies reveal that CAV1 is involved in metabolic alterations – a critical strategy adopted by cancer cells to their survival advantage. Consequently, research findings suggest that CAV1, which is altered in several cancer types, influences tumour development or progression by controlling metabolism. Understanding the molecular interplay between CAV1 and metabolism could help uncover druggable metabolic targets or pathways of clinical relevance in cancer therapy. Here we review from a cancer perspective, the findings that CAV1 modulates cell metabolism with a focus on glycolysis, mitochondrial bioenergetics, glutaminolysis, fatty acid metabolism, and autophagy.
Highlights
Cancer cells have anomalous metabolic features, which enable them to adapt to constraints in the microenvironment [1, 2]
While aerobic glycolysis largely holds true in several tumours, it is known that tumours retain normal mitochondrial function, using glutaminolysis to support proliferation via tricarboxylic acid (TCA) cycle [5, 6]
Similar discrepancies exist in autophagy, where different studies show that both loss and overexpression of CAV1 induces the lysosomal marker light chain 3 beta (LC3B)
Summary
Cancer cells have anomalous metabolic features, which enable them to adapt to constraints in the microenvironment [1, 2]. And contrary to its tumour promoting function highlighted above [37], high CAV1 expression improved overall survival in liver cancer patients, ostensibly by countering eNOS activity [42]. CAV1 expressing colon cancer cells undergo increased glycolysis upon exposure to inhalation anaesthesia (isoflurane), and are protected from tumour necrosis factor associated apoptosis [47].
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
