Transcriptional dysregulation of base excision repair proteins in breast cancer

Griffin Wright; Natalie R Gassman

doi:10.1016/j.dnarep.2020.102922

Transcriptional dysregulation of base excision repair proteins in breast cancer

DNA Repair (Amst). 2020 Sep:93:102922. doi: 10.1016/j.dnarep.2020.102922. Epub 2020 Jul 7.

Authors

Griffin Wright¹, Natalie R Gassman¹

Affiliation

¹ Department of Physiology and Cell Biology, University of South Alabama College of Medicine, Mobile, AL, USA; Mitchell Cancer Institute, University of South Alabama, Mobile, AL, USA.

PMID: 33087263
DOI: 10.1016/j.dnarep.2020.102922

Abstract

Base excision repair (BER) addresses the numerous base lesions and strand breaks induced by exogenous and endogenous stressors daily. The complexity and importance of BER requires careful regulation of basal levels of these proteins and inducible responses following DNA damage. Several reports have noted the dysregulation of BER proteins and defects in BER capacity in cancer. Modulated gene and protein expression of several BER proteins, including APE1, PARP1, POL β, and XRCC1, have been observed in breast cancer. Overexpression of these factors has been associated with chemoresistance and cancer aggressiveness, but the regulatory mechanisms that drive overexpression have not been defined. Here, we review the known transcriptional regulators of these key BER proteins and examine potential mechanisms that may drive overexpression in breast cancer.

Publication types

Research Support, Non-U.S. Gov't
Review

MeSH terms

Breast Neoplasms / genetics*
Breast Neoplasms / metabolism
DNA Repair / genetics*
DNA Repair Enzymes / genetics*
Drug Resistance, Neoplasm
Female
Gene Expression Regulation, Neoplastic*
Humans
Transcription, Genetic*

Substances

DNA Repair Enzymes