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Updated: Jan 21, 2026

Evaluation of Colorectal Cancer Risk and Prevalence by Stool DNA Integrity Detection
Published on: June 8, 2020
Oncogenic splicing abnormalities induced by DEAD-Box Helicase 56 amplification in colorectal cancer
Yuta Kouyama1,2, Takaaki Masuda1, Atsushi Fujii1
1Department of Surgery, Kyushu University Beppu Hospital, Oita, Japan.
Abstract:
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 DDX56 on Ch.7p by a bioinformatics approach using The Cancer Genome Atlas (TCGA) dataset of colorectal cancer (CRC). DDX56 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 DDX56 were explored by gene set enrichment analysis (GSEA), and cell proliferation in vitro and in vivo, cell cycle assays, and using DDX56-knockdown or overexpressed CRC cells. RNA sequencing was carried out to elucidate the effect of DDX56 on mRNA splicing. We found that DDX56 expression was positively correlated with the amplification of DDX56 and was upregulated in CRC cells. High DDX56 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 DDX56 promoted proliferation ability through regulating the cell cycle. DDX56 knockdown reduced intron retention and tumor suppressor WEE1 expression, which functions as a G2-M DNA damage checkpoint. We have identified DDX56 as a novel oncogene and prognostic biomarker of CRC that promotes alternative splicing of WEE1.
Insights
DEAD-Box Helicase 56 (DDX56) is a novel oncogene in colorectal cancer (CRC). Upregulated DDX56 promotes CRC cell proliferation and is a poor prognostic biomarker.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Alternative splicing, regulated by DEAD-Box Helicase (DDX) proteins, is crucial in cancer development.
- The specific role of the DDX family, particularly DDX56, in colorectal cancer (CRC) remains incompletely understood.
Purpose of the Study:
- To investigate DDX56 as a potential oncogene and prognostic biomarker in colorectal cancer.
- To elucidate the molecular mechanisms by which DDX56 influences CRC progression.
Main Methods:
- Bioinformatic analysis of The Cancer Genome Atlas (TCGA) dataset for colorectal cancer.
- Quantitative real-time PCR (RT-qPCR) and immunohistochemical staining to assess DDX56 expression in patient samples.
- In vitro and in vivo assays, gene set enrichment analysis (GSEA), and RNA sequencing to study DDX56 function and its effect on mRNA splicing.
Main Results:
- DDX56 was identified as a candidate oncogene on chromosome 7p and found to be upregulated in CRC cells, correlating with gene amplification.
- High DDX56 expression was significantly associated with lymphatic invasion, distant metastasis, and served as an independent poor prognostic factor in CRC patients.
- DDX56 promoted cell proliferation by regulating the cell cycle and was found to influence alternative splicing, specifically reducing WEE1 expression.
Conclusions:
- DDX56 is a novel oncogene and a valuable prognostic biomarker for colorectal cancer.
- DDX56 promotes CRC progression through regulating the cell cycle and alternative splicing of the WEE1 gene, a critical component of the G2-M DNA damage checkpoint.
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