Feng Yang
Baylor College of Medicine, TX·Medicine & Clinical Research
Prostate cancer depends on the androgen receptor (AR), a protein that responds to male hormones and switches on growth genes. Many tumors eventually grow despite hormone-blocking therapy, a lethal stage called castration-resistant prostate cancer (CRPC), and some then stop responding to taxane chemotherapy drugs such as docetaxel.
- Fields
Medicine & Clinical Research
Biochemistry
Pharmacology
- Topics
prostate cancer
PCa
taxane resistance
- Grants
- 1 known grant, through Apr 2028
What they work on
- Determine how COP1, an E3 ubiquitin ligase, binds and tags GATA2 for degradation in prostate cancer cells, including castration-resistant and taxane-resistant models.
- Test how COP1 controls androgen receptor (AR) levels, AR activity and AR-positive tumor growth, separating GATA2-dependent from GATA2-independent effects, and relate COP1, GATA2 and AR levels in human prostate cancer tissues.
- Test whether COP1 restores docetaxel sensitivity in AR-positive and AR-negative taxane-resistant castration-resistant prostate cancer, and whether this depends on reversing GATA2 overexpression.
More about the research
GATA2, a transcription factor that helps turn on AR and drives tumor growth and drug resistance, is an attractive target but is hard to block directly. A different strategy is to make cells destroy GATA2 faster. This project asks whether COP1, an E3 ubiquitin ligase (an enzyme that tags proteins for destruction), is the enzyme that removes GATA2 in prostate cancer.
Why it matters
Men with advanced prostate cancer that no longer responds to hormone therapy or taxane chemotherapy have few options. Showing that COP1 destroys GATA2 could support a treatment strategy based on boosting GATA2 breakdown rather than blocking it directly. This could help slow tumor growth and restore sensitivity to docetaxel in castration-resistant disease.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Scott Dehm
University of Minnesota, MN·Medicine & Clinical Research
Determine how AR-blocking therapies induce KLF5, a stem cell transcription factor, and lineage plasticity traits in castration-resistant prostate cancer cells.
Susan Logan
New York University, NY·Pharmacology
Test whether macrocycle 13, a synthetic ring-shaped molecule designed to block beta-catenin from binding its DNA partner TCF, suppresses Wnt/beta-catenin signaling in in vivo models of castration-resistant prostate cancer.
Kexin Xu
University of Virginia, VA·Biochemistry
Examine how the m6A-adding enzyme METTL3 binds the nuclear pore protein NUP93 to speed export of m6A-marked mRNAs, using single-molecule microscopy and epitranscriptome-editing tools.
The school
Baylor College of Medicine: 38 labs on PI Pages, $881M a year on research, 115 research doctorates a year.
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