SPOP in Prostate Cancer
Dr. Huang's Cancer Epigenetics and Functional Genomics Lab uses multiple approaches, including gene knockin, to understand how mutations in the gene encoding Speckle-type POZ protein (SPOP) promote prostate tumorigenesis, aberrant androgen receptor transcriptional activity, genomic instability and therapy resistance.
SPOP is the most commonly mutated tumor suppressor gene in human primary prostate cancer. Results from The Cancer Genome Atlas (TCGA) studies show that SPOP-mutated prostate cancers possess the highest transcriptional activity of androgen receptor. This observation can be explained, at least in part, by findings from Dr. Huang's lab showing that SPOP mutations lead to dysregulated proteasome degradation of a number of proteins such as androgen receptor, ERG (a pioneering factor of AR) and BRD4 (a master regulator of transcription).
Findings from the lab's research on SPOP could allow for development of new therapeutics tailored for SPOP-mutated prostate cancer.
All SPOP-related studies in Dr. Huang's lab are supported by Mayo Clinic institutional funds.