USP16 regulates castration-resistant prostate cancer cell proliferation by deubiquitinating and stablizing c-Myc.

ABSTRACT:

Background

c-Myc, a well-established oncogene, plays an important role in the initiation and progression of various cancers, including prostate cancer. However, its mechanism in cancer cell remains largely unknown and whether there exist a deubiquitinase targeting c-Myc also remains elusive.

Methods

Bioinformatic analysis and shRNA screening methods were used to identify potential deubiquitinases that correlate with c-Myc gene signature. Cell proliferation and viability were measured by Cell-Counting-Kit 8 and colony formation assays. A mouse xenograft model of PC3 cells was established to confirm the function of USP16 in vivo. The interaction between USP16 and c-Myc protein was assessed by co-immunoprecipitation and protein co-localization assays. Immunohistochemistry stain

SUBMITTER: Ge J 

PROVIDER: S-EPMC7866668 | biostudies-literature | 2021 Feb

REPOSITORIES: biostudies-literature