Yu Sha-Sha, Tu Yi, Xu Lin-Lin, Tao Xue-Qin, Xu Shan, Wang Shan-Shan, Xiong Yi-Feng, Mei Jin-Hong
Department of Pathology, The First Affiliated Hospital of Nanchang University, Nanchang, China E-mail :
Asian Pac J Cancer Prev. 2015;16(1):175-9. doi: 10.7314/apjcp.2015.16.1.175.
Rad51, a key factor in the homologous recombination pathway for the DNA double-strand break repair, plays a vital role in genesis of non-small-cell lung cancer (NSCLC). In recent years, more and more studies indicate that high expression of Rad51 is of great relevance to resistance of NSCLC to chemotherapeutic agents and ionizing radiation. However, the underlying molecular mechanisms are poorly understood. In this study, we investigated the role of single Rad51 on cell viability in vitro. Our results show that depletion of endogenous Rad51 is sufficient to inhibit the growth of the A549 lung cancer cell line, by accumulating cells in G1 phase and inducing cell death. We conclude that independent Rad51 expression is critical to the survival of A549 cells and can be an independent prognostic factor in NSCLC patients.
Rad51是DNA双链断裂修复同源重组途径中的关键因子，在非小细胞肺癌（NSCLC）的发生中起重要作用。近年来，越来越多的研究表明，Rad51的高表达与NSCLC对化疗药物和电离辐射的耐药性密切相关。然而，其潜在的分子机制尚不清楚。在本研究中，我们研究了单个Rad51对体外细胞活力的作用。我们的结果表明，内源性Rad51的缺失足以抑制A549肺癌细胞系的生长，使细胞在G1期积累并诱导细胞死亡。我们得出结论，独立的Rad51表达对A549细胞的存活至关重要，并且可能是NSCLC患者的一个独立预后因素。
