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首页> 外文期刊>Cell cycle >Chemotherapy-induced p53-dependent and -independent DNA damage responses are enhanced by poly(ADP-ribose) polymerase (PARP) inhibition in BRCA-proficient cancer cells
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Chemotherapy-induced p53-dependent and -independent DNA damage responses are enhanced by poly(ADP-ribose) polymerase (PARP) inhibition in BRCA-proficient cancer cells

机译：化疗诱导的p53依赖性和非依赖性DNA损伤反应通过BRCA熟练癌细胞中的聚（ADP-核糖）聚合酶（PARP）抑制得到增强

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摘要

Poly(ADP-ribose) polymerase (PARP) was first recognized to be important for the repair of broken DNA strands in 1980,1 when PARP inhibitors were suggested as DNA damage sensitizing agents. Blocking DNA repair through PARP inhibition could potentially increase tumor cell kill and enhance the efficacy of chemotherapy and 7-irradiation2 or allow these treatments to be used at lower doses with reduced toxicities. Sensitization of normal cells represents an important caveat. However, genomic instability, uncontrolled cell division and alterations in proteins important for survival after exposure to DNA damage, such as p53, may render cancer cells more sensitive to combination therapy than non-transformed cells. These questions are under active investigation.
机译：聚（ADP-核糖）聚合酶（PARP）在1980年首次被认为对修复断裂的DNA链很重要1，当时有人建议使用PARP抑制剂作为DNA损伤敏感剂。通过抑制PARP来阻止DNA修复可能会增加肿瘤细胞的杀伤力，并增强化学疗法和7辐射2的疗效，或者允许以较低的剂量使用这些治疗方法，同时降低毒性。正常细胞的敏化是一个重要的警告。但是，基因组不稳定性，不受控制的细胞分裂以及对DNA损伤后存活至关重要的蛋白质的改变（例如p53）可能使癌细胞比非转化细胞对联合治疗更为敏感。这些问题正在积极调查中。

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