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The  DEAD ‐box‐protein  DDX 5 is an  ATP ‐dependent  RNA  helicase that is frequently overexpressed in various cancers and acts as a transcriptional co‐activator of several transcription factors, including β‐catenin.  DDX 5 is reported to be involved in cancer progression by promoting cell proliferation and epithelial–mesenchymal transition. However, the clinical significance and biological role of  DDX 5 in non‐small‐cell lung cancer ( NSCLC ) remain largely unknown. In this study, we examined the expression of  DDX 5 in clinical  NSCLC  samples, investigated its role in regulating  NSCLC  cell proliferation and tumorigenesis, and explored the possible molecular mechanism. We found that  DDX 5 was significantly overexpressed in  NSCLC  tissues as compared with the matched normal adjacent tissues. In addition, overexpression of  DDX 5 was associated with advanced clinical stage, higher Ki67 index, and shorter overall survival in  NSCLC  patients. Upregulation of  DDX 5 promoted proliferation of  NSCLC  cells  in vitro  and growth of  NSCLC  xenografts  in vivo , whereas downregulation of  DDX 5 showed the opposite effects. Furthermore,  DDX 5 directly interacted with β‐catenin, promoted its nuclear translocation, and co‐activated the expression of cyclin D1 and c‐Myc. β‐catenin silencing significantly abrogated  DDX 5‐induced cyclin D1 and c‐Myc expression and proliferation in  NSCLC  cells. Interestingly,  DDX 5 and cyclin D1 expression followed positive correlation in the same set of  NSCLC  samples. These findings indicated that  DDX 5 played an important role in the proliferation and tumorigenesis of  NSCLC  cells by activating the β‐catenin signaling pathway. Therefore,  DDX 5 may serve as a novel prognostic marker and potential therapeutic target in the treatment of  NSCLC .

DDX 5 promotes proliferation and tumorigenesis of non‐small‐cell lung cancer cells by activating β‐catenin signaling pathway