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http://dx.doi.org/10.7314/APJCP.2015.16.1.175

Effects of Rad51 on Survival of A549 Cells  

Yu, Sha-Sha (Department of Pathology, The First Affiliated Hospital of Nanchang University)
Tu, Yi (Department of Pathology, The First Affiliated Hospital of Nanchang University)
Xu, Lin-Lin (Department of Scientific Research Center, The First Affiliated Hospital of Nanchang University)
Tao, Xue-Qin (Department of Pathology, The First Affiliated Hospital of Nanchang University)
Xu, Shan (Department of Pathology, The First Affiliated Hospital of Nanchang University)
Wang, Shan-Shan (Department of Pathology, The First Affiliated Hospital of Nanchang University)
Xiong, Yi-Feng (Department of Pathology, The First Affiliated Hospital of Nanchang University)
Mei, Jin-Hong (Department of Pathology, The First Affiliated Hospital of Nanchang University)
Publication Information
Asian Pacific Journal of Cancer Prevention / v.16, no.1, 2015 , pp. 175-179 More about this Journal
Abstract
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.
Keywords
Rad51; A549 cell; cell survival;
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