RAD52 motif‑containing protein 1 promotes non‑small cell lung cancer cell proliferation and survival via cell cycle regulation.

DNA repair proteins such as RAD52 have been implicated in tumor progression and response to chemotherapy. RAD52 motif-containing protein 1 (RDM1) has been implicated in the response to chemotherapeutic agent cisplatin; however, its function in lung cancer progression remains unclear. This study aimed to investigate the role of RDM1 in the progression of non-small cell lung cancer (NSCLC). We found elevated RDM1 mRNA and protein expression in NSCLC tissues and cell lines compared to levels in normal lung cells. RDM1 protein expression in lung cancer tissues was found to correlate with tumor size, histological differentiation, lymph node metastasis and tumor-node-metastasis (TNM) stage. Knockdown of the RDM1 gene with siRNA significantly reduced the cellular proliferation rate and increased apoptosis in the human NSCLC cell line, NCI-H1299. Compared to wild-type NCI-H1299 cells, RDM1 knockdown enhanced the activity of caspase-3 and caspase-7, and decreased the proportion of cells in the S-phase of the cell cycle. Taken together, these data imply that RDM1 promotes the survival and proliferation of NSCLC cells. Due to its similarity to RAD52, we hypothesized that RDM1 potentially repairs DNA double-strand breaks arising through DNA replication, thereby preventing G(2)/M cell cycle arrest. Accordingly, specific targeting of RDM1 may be a novel therapeutic strategy in the treatment of NSCLC.