错误:搜索内容不能为空,请输入英文关键词
错误:关键词超出字数限制,请精简
高级检索

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

  • Yunshu Shi,
  • Junyong Wang,
  • Qiang Yuan,
  • Yingying Chen,
  • Miao Zhao,
  • Xiaoyu Li,
  • Zitong Wang,
  • Hao Zhou,
  • Fangli Zhu,
  • Bing Wei,
  • Yanan Jiang,
  • Jimin Zhao,
  • Yan Qiao,
  • Zigang Dong,
  • Kangdong Liu

摘要

Novel therapeutic targets and their inhibitors for esophageal squamous cell carcinoma (ESCC) prevention and therapy are urgently needed. This study aimed to investigate the function of DEAD-box helicase 5 (DDX5) in ESCC progression and to identify a promising inhibitor of DDX5. We verified that DDX5 was highly expressed in ESCC and played an oncogenic role, binding with vav guanine nucleotide exchange factor 3 (VAV3) mRNA and facilitating VAV3 mRNA N6-methyladenosine (m6A) modification by interacting with the m6A methyltransferase 3 (METTL3). M6A-modified VAV3 mRNA was identified by insulin-like growth factor 1 (IGF2BP1), increasing mRNA stability. Methylnissolin-3-β-D-O-glucoside (MD) inhibited ESCC progression through the DDX5-VAV3 axis. Our findings suggest that DDX5 promotes ESCC progression. MD inhibits ESCC progression by targeting DDX5.