In cancer treatment, chemotherapy is one of the main strategies used. The knowledge of the cellular and molecular characteristics of tumors allows the use of more specific drugs, making the removal of tumors more efficient. Among the drugs of choice in these treatments, topoisomerase inhibitors are widely used against different types of tumors. Topoisomerases are enzymes responsible for maintaining the structure of DNA, altering its topological state temporarily during the processes of replication and transcription, in order to avoid supercoiling and entanglements at the double helix. The DNA damage formed as a result of topoisomerase inhibition can be repaired by DNA repair mechanisms. Thus, DNA repair pathways can modulate the effectiveness of chemotherapy. Homologous recombination (HR) and non-homologous end joining (NHEJ) are the main pathways involved in the removal of double strand breaks (DSBs); while nucleotide excision repair (NER) is mainly characterized by the removal of lesions that lead to significant structural distortions in the DNA double helix. Evidence has shown that DSBs are the main type of damage resulting from the inhibition of the DNA topoisomerase II enzyme, and therefore the involvement of HR and NHEJ pathways in the repair process is well established. However, some topoisomerase II inhibitors induce other types of lesions, like DNA adducts, interstrand crosslinks and reactive oxygen species, and studies have shown that other DNA repair pathways might be participating in removing injury induced by these drugs. This review aims to correlate the involvement of proteins from different DNA repair pathways in response to these drugs, with an emphasis on NER.

中文翻译：

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核苷酸切除修复蛋白在响应拓扑异构酶II抑制剂诱导的DNA损伤中的作用。

在癌症治疗中，化学疗法是使用的主要策略之一。肿瘤的细胞和分子特征的知识允许使用更具体的药物，从而使肿瘤的清除更加有效。在这些治疗中选择的药物中，拓扑异构酶抑制剂被广泛用于治疗不同类型的肿瘤。拓扑异构酶是负责维持DNA结构，在复制和转录过程中暂时改变其拓扑状态的酶，以避免双螺旋的超螺旋和缠结。拓扑异构酶抑制作用形成的DNA损伤可以通过DNA修复机制修复。因此，DNA修复途径可以调节化学疗法的有效性。同源重组（HR）和非同源末端连接（NHEJ）是去除双链断裂（DSB）的主要途径。而核苷酸切除修复（NER）的主要特征是去除了导致DNA双螺旋结构发生明显结构变形的损伤。有证据表明，DSB是由DNA拓扑异构酶II酶的抑制引起的主要损害类型，因此，HR和NHEJ途径参与修复过程已得到充分证实。但是，某些拓扑异构酶II抑制剂会诱导其他类型的损伤，例如DNA加合物，链间交联和活性氧，并且研究表明，其他DNA修复途径可能参与清除这些药物引起的损伤。