A5055802892- Prostate Cancer Treatment and Research
- Cancer-related gene regulation
- Protein Degradation and Inhibitors
- Ubiquitin and proteasome pathways
- Cancer-related Molecular Pathways
- Cancer-related molecular mechanisms research
University of Maryland, Baltimore
2023-2025
University of Baltimore
2025
University of Maryland Marlene and Stewart Greenebaum Comprehensive Cancer Center
2023-2024
Sidney Kimmel Comprehensive Cancer Center
2023
University of Mary
2023
Abstract Overexpression of androgen receptor (AR) is the primary cause castration-resistant prostate cancer, although mechanisms upregulating AR transcription in this context are not well understood. Our RNA-seq studies revealed that SMAD3 knockdown decreased levels and target genes, whereas SMAD4 or SMAD2 had little no effect. ChIP-seq analysis showed global binding to chromatin. Mechanistically, we show binds intron 3 gene promote expression. Targeting these sites by CRISPRi reduced...
Abstract Epigenetic regulation plays a crucial role in the development and progression of prostate cancer. JMJD1A (also called KDM3A) promotes cancer by upregulating gene expression through removal repressive H3K9 methylation marks. Here, we found for glutamine biosynthesis cells. knockdown (KD) significantly reduced cellular levels inhibited cell growth under glutamine-deprivation conditions. RNA-seq studies showed that KD GLUL, key enzyme de novo synthesis. mRNA GLUL were positively...
Androgen receptor (AR) is a main driver for castration-resistant prostate cancer (CRPC). c-Myc an oncogene underlying tumorigenesis. Here, we find that the deubiquitinase USP11 targets both AR and in (PCa). expression was up-regulated metastatic PCa CRPC. knockdown (KD) significantly inhibited cell growth. Our RNA-seq studies revealed as top transcription factors altered after KD. ChIP-seq analysis showed either KD or replacement of endogenous with catalytic-inactive mutant decreased...
Abstract Overexpression of the androgen receptor (AR) is primary cause development castration-resistant prostate cancer (CRPC), although mechanisms upregulating AR transcription in this context are not well understood. Our RNA-seq analysis revealed as top pathway altered after SMAD3 knockdown cells. decreased levels AR, AR-V7 and target gene transcripts, whereas SMAD4 or SMAD2 had little no effect. ChIP-seq showed that global binding to chromatin. Mechanistically, we show binds intron 3...