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The RNA-binding protein DDX39B promotes colorectal adenocarcinoma progression by stabilizing DCLK1

  • 0Department of Clinical Laboratory, Qilu Hospital of Shandong University, No. 107, Wenhua West Road, Lixia District, Jinan Shandong Province 250012, P.R. China.
Human Molecular Genetics +

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June 30, 2025

|

June 30, 2025

View abstract on PubMed

Summary

This summary is machine-generated.

DEAD-box helicase DDX39B promotes colon adenocarcinoma (COAD) growth and metastasis by stabilizing DCLK1-B mRNA. Targeting DDX39B may offer a new therapeutic strategy for COAD patients.

Area Of Science

  • Molecular Biology
  • Oncology
  • RNA Biology

Background

  • DEAD-box (DDX) RNA helicases regulate key cellular processes.
  • DDX39B is implicated in various pathologies, including cancer.
  • The role of DDX39B in colon adenocarcinoma (COAD) requires further elucidation.

Purpose Of The Study

  • To investigate the functional role of DDX39B in COAD proliferation and metastasis.
  • To uncover the molecular mechanisms underlying DDX39B's function in COAD.
  • To evaluate DDX39B as a potential therapeutic target for COAD.

Main Methods

  • Analysis of DDX39B expression in COAD tissues.
  • In vitro and in vivo functional assays to assess proliferation and metastasis.
  • Investigation of DDX39B's association with Ki67 and epithelial-mesenchymal transition (EMT).
  • Assessment of DDX39B's effect on DCLK1-B mRNA stability and protein expression.
  • DCLK1-B silencing experiments.

Main Results

  • DDX39B was significantly upregulated in COAD tissues, correlating with poor prognosis.
  • DDX39B overexpression enhanced COAD cell proliferation and metastasis.
  • DDX39B facilitated EMT and was positively associated with Ki67 levels.
  • DDX39B increased DCLK1-B mRNA stability and protein levels, promoting cancer stemness.
  • Silencing DCLK1-B reversed the pro-metastatic effects of DDX39B.

Conclusions

  • DDX39B acts as an oncogene in COAD by promoting proliferation, metastasis, and EMT.
  • DDX39B enhances COAD progression via stabilizing DCLK1-B mRNA, thereby increasing cancer stemness.
  • DDX39B represents a promising therapeutic target for colon adenocarcinoma.

Keywords:

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