Nature Communications (Aug 2020)
Caveolin-1-mediated sphingolipid oncometabolism underlies a metabolic vulnerability of prostate cancer
- Jody Vykoukal,
- Johannes F. Fahrmann,
- Justin R. Gregg,
- Zhe Tang,
- Spyridon Basourakos,
- Ehsan Irajizad,
- Sanghee Park,
- Guang Yang,
- Chad J. Creighton,
- Alia Fleury,
- Jeffrey Mayo,
- Adriana Paulucci-Holthauzen,
- Jennifer B. Dennison,
- Eunice Murage,
- Christine B. Peterson,
- John W. Davis,
- Jeri Kim,
- Samir Hanash,
- Timothy C. Thompson
Affiliations
- Jody Vykoukal
- Department of Clinical Cancer Prevention, The University of Texas MD Anderson Cancer Center
- Johannes F. Fahrmann
- Department of Clinical Cancer Prevention, The University of Texas MD Anderson Cancer Center
- Justin R. Gregg
- Department of Urology, The University of Texas MD Anderson Cancer Center
- Zhe Tang
- Department of Genitourinary Medical Oncology, The University of Texas MD Anderson Cancer Center
- Spyridon Basourakos
- Department of Genitourinary Medical Oncology, The University of Texas MD Anderson Cancer Center
- Ehsan Irajizad
- Department of Biostatistics, The University of Texas MD Anderson Cancer Center
- Sanghee Park
- Department of Genitourinary Medical Oncology, The University of Texas MD Anderson Cancer Center
- Guang Yang
- Department of Genitourinary Medical Oncology, The University of Texas MD Anderson Cancer Center
- Chad J. Creighton
- Department of Bioinformatics and Computational Biology, The University of Texas MD Anderson Cancer Center
- Alia Fleury
- Department of Clinical Cancer Prevention, The University of Texas MD Anderson Cancer Center
- Jeffrey Mayo
- Department of Clinical Cancer Prevention, The University of Texas MD Anderson Cancer Center
- Adriana Paulucci-Holthauzen
- Department of Genetics, The University of Texas MD Anderson Cancer Center
- Jennifer B. Dennison
- Department of Clinical Cancer Prevention, The University of Texas MD Anderson Cancer Center
- Eunice Murage
- Department of Clinical Cancer Prevention, The University of Texas MD Anderson Cancer Center
- Christine B. Peterson
- Department of Biostatistics, The University of Texas MD Anderson Cancer Center
- John W. Davis
- Department of Urology, The University of Texas MD Anderson Cancer Center
- Jeri Kim
- Department of Genitourinary Medical Oncology, The University of Texas MD Anderson Cancer Center
- Samir Hanash
- Department of Clinical Cancer Prevention, The University of Texas MD Anderson Cancer Center
- Timothy C. Thompson
- Department of Genitourinary Medical Oncology, The University of Texas MD Anderson Cancer Center
- DOI
- https://doi.org/10.1038/s41467-020-17645-z
- Journal volume & issue
-
Vol. 11,
no. 1
pp. 1 – 16
Abstract
The mechanisms associated with Caveolin-1 (Cav-1) mediated metabolic changes in prostate cancer are unclear. Here, the authors show that Cav-1 promotes rewiring of cancer cell lipid metabolism towards a program of exogenous lipid scavenging and vesicle biogenesis that intersects with mitochondrial dynamics in prostate tumors.
