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DNA损伤反应在维持细胞基因组稳定性和机体存活发挥重要作用。DNA双链断裂(Double strand breaks,DSBs)是DNA损伤最严重的形式。同源重组修复是体内参与DSBs损伤修复的重要机制之一,其中Rad51是体内参与同源重组性DNA修复的关键因子。Rad51在人类的多种肿瘤组织中高表达,如乳腺癌、非小细胞肺癌、前列腺癌等,与肿瘤的转移和恶化相关。如何有效下调肿瘤组织中的Rad51的水平,降低肿瘤细胞的DNA损伤修复能力,从而提高肿瘤治疗的疗效具有潜在的临床应用价值。本文对近年来的一个研究热点靶向Rad51在肿瘤治疗研究中的应用进行综述。
DNA damage response plays an important role in maintaining cell genome stability and body survival. DNA double strand breaks (DSBs) are the most damaging forms of DNA damage. Homologous recombination repair is one of the important mechanisms involved in DSBs injury repair in vivo, and Rad51 is the key factor involved in the homologous recombination DNA repair in vivo. Rad51 is highly expressed in many human tumor tissues, such as breast cancer, non-small cell lung cancer, prostate cancer, and the like, and is associated with tumor metastasis and deterioration. How to effectively down-regulate the level of Rad51 in tumor tissue, reduce the DNA damage repair ability of tumor cells and improve the curative effect of tumor therapy has potential clinical application value. This review summarizes the application of Rad51 targeting tumor therapy in recent years.