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.
DNA Repair (Amst). 2020 Sep;93:102922. doi: 10.1016/j.dnarep.2020.102922. Epub 2020 Jul 7.
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.
碱基切除修复 (BER) 可处理由外源和内源应激因素每天诱导产生的众多碱基损伤和链断裂。BER 的复杂性和重要性要求对这些蛋白质的基础水平和 DNA 损伤后的诱导反应进行精细调控。一些研究报告指出，BER 蛋白失调以及 BER 能力缺陷与癌症有关。在乳腺癌中观察到几种 BER 蛋白（包括 APE1、PARP1、POLβ 和 XRCC1）的基因和蛋白表达发生调节。这些因素的过表达与化疗耐药性和癌症侵袭性有关，但尚未确定驱动过表达的调节机制。在这里，我们综述了这些关键 BER 蛋白的已知转录调节因子，并探讨了可能导致乳腺癌中过表达的潜在机制。
