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 studiesindicate that high expression of Rad51 is of great relevance to resistance of NSCLC to chemotherapeutic agentsand 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 endogenousRad51 is sufficient to inhibit the growth of the A549 lung cancer cell line, by accumulating cells in G1 phase andinducing cell death. We conclude that independent Rad51 expression is critical to the survival of A549 cells andcan be an independent prognostic factor in NSCLC patients.
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