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Published on: April 28, 2021
Transcriptional dysregulation of base excision repair proteins in breast cancer
Griffin Wright1, Natalie R Gassman1
1Department 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.
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.
Insights
Base excision repair (BER) proteins are crucial for DNA repair but are often overexpressed in breast cancer. This review explores transcriptional regulators potentially driving this overexpression, impacting chemoresistance and cancer aggressiveness.
Area of Science:
- Molecular Biology
- Genetics
- Oncology
Background:
- Base excision repair (BER) is vital for repairing DNA damage from daily stressors.
- Dysregulation and defects in BER capacity are observed in various cancers.
- Specific BER proteins like APE1, PARP1, POL β, and XRCC1 show altered expression in breast cancer.
Purpose of the Study:
- To review known transcriptional regulators of key BER proteins.
- To examine potential mechanisms driving BER protein overexpression in breast cancer.
- To understand the link between BER protein overexpression, chemoresistance, and cancer aggressiveness.
Main Methods:
- Literature review of transcriptional regulators of BER proteins.
- Analysis of studies reporting BER protein expression in breast cancer.
- Examination of potential regulatory mechanisms for overexpression.
Main Results:
- Several BER proteins (APE1, PARP1, POL β, XRCC1) are modulated in breast cancer.
- Overexpression of these proteins correlates with chemoresistance and aggressiveness.
- Mechanisms driving this overexpression remain largely undefined.
Conclusions:
- Understanding BER protein regulation is critical for breast cancer therapy.
- Identifying transcriptional drivers of overexpression may reveal new therapeutic targets.
- Further research is needed to elucidate regulatory mechanisms and their clinical implications.
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