SPOP promotes ATF2 ubiquitination and degradation to suppress prostate cancer progression.

ABSTRACT:

Background

Next-generation sequencing of the exome and genome of prostate cancers has identified numerous genetic alterations. SPOP (Speckle-type POZ Protein) is one of the most frequently mutated genes in primary prostate cancer, suggesting that SPOP may be a potential driver of prostate cancer. The aim of this work was to investigate how SPOP mutations contribute to prostate cancer development and progression.

Methods

To identify molecular mediators of the tumor suppressive function of SPOP, we performed a yeast two-hybrid screen in a HeLa cDNA library using the full-length SPOP as bait. Immunoprecipitation and Western Blotting were used to analyze the interaction between SPOP and ATF2. Cell migration and invasion were determined by Transwell assays. Immunohistochemistry w

SUBMITTER: Ma J 

PROVIDER: S-EPMC6042370 | biostudies-literature | 2018 Jul

REPOSITORIES: biostudies-literature