ArticleCancer cell international2024
DDX19A promotes gastric cancer cell proliferation and migration by activating the PI3K/AKT pathway.
Article in Cancer cell international, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Homoharringtonine suppresses gastric cancer progression by targeting PI3K/ AKT/FOXO pathway and impairing the GSH-GPX4 antioxidant axis.Cancer chemotherapy and pharmacology · 2026Article
- DDX10 RNA Helicase: Structure, Function, and Oncogenic Roles Across Solid and Hematologic Tumors.Genes · 2026Review
- Mechanism of Platelet-Rich Plasma in Promoting Diabetic Wound Healing via the PI3K/AKT Signaling Pathway to Regulate Collagen Synthesis and Angiogenesis.Journal of diabetes research · 2026Article
- Knockdown of CTMP Enhances Progesterone Sensitivity in Endometrial Cancer by Inhibiting the PI3K/AKT Signaling Pathway.Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
- DNA methyltransferase 3A: A prognostic biomarker and potential target for immunotherapy in gastric cancer.Medicine · 2025Article
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Authors and funding
7 authors.
Funding
Abstract
backgroundDEAD-box RNA helicase 19 A (DDX19A) is overexpressed in cervical squamous cell carcinoma. However, its role in gastric cancer remains unclear. The present study aimed to explore the role and underlying mechanism of DDX19A in the development of gastric cancer.
methodsThe expression of DDX19A in gastric cancer and paracancerous tissues was evaluated through quantitative polymerase chain reaction, western blotting, and immunohistochemical staining. The biological functions of DDX19A in gastric cancer were determined using CCK8, plate colony-forming, and Transwell migration assays. The specific mechanism of DDX19A in gastric cancer cells was studied using western blotting, RNA-binding protein immunoprecipitation, mRNA half-life detection, and nuclear and cytoplasmic RNA isolation.
resultsDDX19A was highly expressed in gastric cancer and positively associated with malignant clinicopathological features and poor prognosis. Additionally, DDX19A promoted gastric cancer cell proliferation, migration, and epithelial-mesenchymal transition phenotypes. Mechanistically, DDX19A activated the PI3K/AKT pathway by upregulating phosphatidylinositol-3-kinase (PIK3CA) expression. Furthermore, DDX19A interacted with PIK3CA mRNA, stabilized it, and facilitated its export from the nucleus.
conclusionsOur study reveals a novel mechanism whereby DDX19A promotes the proliferation and migration of gastric cancer cells by enhancing the stability and nuclear export of PIK3CA mRNA, thereby activating the PI3K/AKT pathway.
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