Journal
CELLS
Volume 11, Issue 15, Pages -Publisher
MDPI
DOI: 10.3390/cells11152329
Keywords
prostate cancer; glucuronidation; African American prostate cancer; androgen signaling; metabolic regulation; tumorigenesis
Categories
Funding
- National Cancer Institute [R01CA267090, R01CA227559, R01CA227559S1, RP210227, P30CA125123]
- Prostate Cancer Research Program Health Disparity Award from the Department of Defense [W81XWH-22-1-0135]
- Integrated Microscopy Core at Baylor College of Medicine
- Center for Advanced Microscopy and Image Informatics (CAMII)
- NIH [DK56338, CA125123, ES030285]
- CPRIT [RP150578, RP170719]
- Prostate Cancer Foundation Challenge Award
- Agilent Technologies Center for Excellence in Mass Spectrometry
- Charles C. Bell Jr. Endowment from Baylor College of Medicine
- Early Investigator Research Award from the Department of Defense
- Canadian Institutes of Health Research [CIHR FRN-408093]
- Cancer Research Society (CRS) [836824]
- Prostate Cancer Canada Rising Star Award [RS2013-55]
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UGT2B28 gene plays a key role in promoting prostate tumor growth, with higher expression levels observed in African American men with prostate cancer and regulated by full-length androgen receptor.
Prostate cancer (PCa) is the second most diagnosed cancer in the United States and is associated with metabolic reprogramming and significant disparities in clinical outcomes among African American (AA) men. While the cause is likely multi-factorial, the precise reasons for this are unknown. Here, we identified a higher expression of the metabolic enzyme UGT2B28 in localized PCa and metastatic disease compared to benign adjacent tissue, in AA PCa compared to benign adjacent tissue, and in AA PCa compared to European American (EA) PCa. UGT2B28 was found to be regulated by both full-length androgen receptor (AR) and its splice variant, AR-v7. Genetic knockdown of UGT2B28 across multiple PCa cell lines (LNCaP, LAPC-4, and VCaP), both in androgen-replete and androgen-depleted states resulted in impaired 3D organoid formation and a significant delay in tumor take and growth rate of xenograft tumors, all of which were rescued by re-expression of UGT2B28. Taken together, our findings demonstrate a key role for the UGT2B28 gene in promoting prostate tumor growth.
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