CDK2-activated TRIM32 phosphorylation and nuclear translocation promotes radioresistance in triple-negative breast cancer.

ABSTRACT:

Introduction

Despite radiotherapy being one of the major treatments for triple-negative breast cancer (TNBC), new molecular targets for its treatment are still required due to radioresistance. CDK2 plays a critical role in TNBC. However, the mechanism by which CDK2 promotes TNBC radioresistance remains to be clearly elucidated.

Objectives

We aimed to elucidate the relationship between CDK2 and TRIM32 and the regulation mechanism in TNBC.

Methods

We performed immunohistochemical staining to detect nuclear TRIM32, CDK2 and STAT3 on TNBC tissues. Western blot assays and PCR were used to detect the protein and mRNA level changes. CRISPR/Cas9 used to knock out CDK2. shRNA-knockdown and transfection assays also used to knock out target genes. GST pull-down analysis, immunop

SUBMITTER: Tang J 

PROVIDER: S-EPMC11258662 | biostudies-literature | 2024 Jul

REPOSITORIES: biostudies-literature