CK2-mediated CCDC106 phosphorylation is required for p53 degradation in cancer progression.

ABSTRACT:

Background

Dysfunction of p53 is a key cause of cancer development, while CCDC106 can reduce p53 stability and is associated with lung cancer. However, the roles of CCDC106 in other cancer types and its upstream regulators have not been investigated.

Methods

The phosphorylation status was investigated by in vitro kinase assay and Western blotting using phosphorylation-specific antibodies. Co-immunoprecipitation assay and GST-pulldown were used to detect protein interaction. Cell viability, apoptosis, colony formation, wound-healing and invasion assays were measured for in vitro functional analyses. The in vivo effect of CCDC106 on tumor growth was investigated using a subcutaneous xenograft tumor mouse model.

Results

We demonstrated that CCDC106 knockdown enhanced apo

SUBMITTER: Ning Y 

PROVIDER: S-EPMC6423756 | biostudies-literature | 2019 Mar

REPOSITORIES: biostudies-literature