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DDX5 promotes esophageal squamous cell carcinoma growth through sustaining VAV3 mRNA stability

Yunshu Shi1,2,3,4, Junyong Wang5, Qiang Yuan1,2,3

  • 1The Pathophysiology Department, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, China.

Oncogene
|September 17, 2024
PubMed

Insights

DEAD-box helicase 5 (DDX5) drives esophageal squamous cell carcinoma (ESCC) progression by regulating VAV3 mRNA stability. Methylnissolin-3-β-D-O-glucoside (MD) shows promise in inhibiting ESCC by targeting DDX5.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Esophageal squamous cell carcinoma (ESCC) requires novel therapeutic strategies.
  • Identifying key molecular drivers and inhibitors is crucial for effective ESCC treatment.

Purpose of the Study:

  • To investigate the role of DEAD-box helicase 5 (DDX5) in ESCC progression.
  • To identify a potential inhibitor targeting DDX5 for ESCC therapy.

Main Methods:

  • Expression analysis of DDX5 in ESCC tissues.
  • Investigating the interaction of DDX5 with VAV3 mRNA and METTL3.
  • Assessing the role of IGF2BP1 in m6A-modified VAV3 mRNA stability.
  • Evaluating the inhibitory effect of Methylnissolin-3-β-D-O-glucoside (MD) on ESCC progression.

Main Results:

  • DDX5 is highly expressed in ESCC and promotes tumor progression.
  • DDX5 facilitates N6-methyladenosine (m6A) modification of VAV3 mRNA via METTL3.
  • IGF2BP1 enhances the stability of m6A-modified VAV3 mRNA.
  • MD treatment inhibits ESCC progression by targeting the DDX5-VAV3 pathway.

Conclusions:

  • DDX5 acts as an oncogene in ESCC progression.
  • The DDX5-VAV3 axis is a critical pathway in ESCC.
  • MD is a potential therapeutic agent for ESCC by inhibiting DDX5.

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