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Alternative splicing, regulated by  DEAD ‐Box Helicase ( DDX ) families, plays an important role in cancer. However, the relationship between the  DDX  family and cancer has not been fully elucidated. In the present study, we identified a candidate oncogene   DDX 56  on Ch.7p by a bioinformatics approach using The Cancer Genome Atlas ( TCGA ) dataset of colorectal cancer ( CRC ).  DDX 56 expression was measured by  RT ‐ qPCR  and immunochemical staining in 108  CRC  patients. Clinicopathological and survival analyses were carried out using three  CRC  datasets. Biological roles of  DDX 56 were explored by gene set enrichment analysis ( GSEA ), and cell proliferation in vitro and in vivo, cell cycle assays, and using   DDX 56 ‐knockdown or overexpressed  CRC  cells.  RNA  sequencing was carried out to elucidate the effect of  DDX 56 on  mRNA  splicing. We found that  DDX 56 expression was positively correlated with the amplification of  DDX 56 and was upregulated in  CRC  cells. High  DDX 56 expression was associated with lymphatic invasion and distant metastasis and was an independent poor prognostic factor. In vitro analysis, in vivo analysis and  GSEA  showed that  DDX 56 promoted proliferation ability through regulating the cell cycle.   DDX 56  knockdown reduced intron retention and tumor suppressor  WEE 1 expression, which functions as a G2‐M  DNA  damage checkpoint. We have identified   DDX 56  as a novel oncogene and prognostic biomarker of  CRC  that promotes alternative splicing of  WEE 1.

Oncogenic splicing abnormalities induced by DEAD ‐Box Helicase 56 amplification in colorectal cancer