BUB1 regulates non-homologous end joining pathway to mediate radioresistance in triple-negative breast cancer.

ABSTRACT:

Background

Triple-negative breast cancer (TNBC) is a highly aggressive form of breast cancer subtype often treated with radiotherapy (RT). Due to its intrinsic heterogeneity and lack of effective targets, it is crucial to identify novel molecular targets that would increase RT efficacy. Here we demonstrate the role of BUB1 (cell cycle Ser/Thr kinase) in TNBC radioresistance and offer a novel strategy to improve TNBC treatment.

Methods

Gene expression analysis was performed to look at genes upregulated in TNBC patient samples compared to other subtypes. Cell proliferation and clonogenic survivals assays determined the IC₅₀ of BUB1 inhibitor (BAY1816032) and radiation enhancement ratio (rER) with pharmacologic and genomic BUB1 inhibition. Mammary fat pad xenografts

SUBMITTER: Sriramulu S 

PROVIDER: S-EPMC11167950 | biostudies-literature | 2024 Jun

REPOSITORIES: biostudies-literature