ArticleMolecular therapy. Oncology2024
Newcastle disease virus harboring the PTEN gene inhibits pancreatic cancer growth by inhibiting PI3K/AKT/mTOR signaling and activating apoptosis.
Article in Molecular therapy. Oncology, 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.
- A PRK-armed oncolytic adenovirus drives calreticulin exposure for dendritic cell licensing to prime antitumor CD8⁺ T cells and synergizes with anti-PD-1 or CAR-T therapy in colorectal cancer.Journal of gastroenterology · 2026Article
- Exploratory Multi-Platform Bioinformatic Analysis of MEAK7 and Its Molecular, Survival, and Immune Associations in Pancreatic Ductal Adenocarcinoma.International journal of molecular sciences · 2026Article
- Genetic Medicine Approaches for Tumor Suppressor Loss: Therapeutic Replacement with Self-Amplifying RNA.Pharmaceutical research · 2026Review
- p53-mediated regulation of electron transport chain and nucleotide synthesis during Newcastle disease virus infection.Journal of virology · 2025Article
- Acid phosphatase type 6 promotes endometrial cancer progression via activating PI3K/AKT pathway.Molecular biology reports · 2025Article
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Authors and funding
8 authors.
Funding
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Abstract
Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive and intractable cancer that requires more effective therapies that can improve early detection, enhance treatment efficacy, and provide better patient outcomes. Kirsten rat sarcoma viral oncogene homolog (KRAS) mutations and reduced phosphatase and tensin homolog (PTEN) protein expression are key factors driving the proliferation and severity of PDAC. To address this, a recombinant Newcastle disease virus (rNDV) containing the PTEN gene (rNDV-PTEN) was created to investigate its PDAC cell-killing and tumor-suppression effects in PDAC cells transplanted into mice. PTEN expression induced by rNDV-PTEN virus infection in KRAS-mutated PDAC cells lowered phosphatidylinositol 3-kinases (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling, promoted PDAC cell death, and suppressed tumor growth. PTEN overexpression promotes apoptotic signaling pathways in both PANC-1 cells and orthotopic xenograft mice. Additionally, during virotherapy, rNDV-PTEN-injected mice exhibited a mild immune response and no abnormal responses in blood parameters such as glucose, triglyceride, and total cholesterol levels. These findings support the potential of rNDV-PTEN as a safe and effective therapy for PDAC with highly activated PI3K/AKT/mTOR signaling caused by KRAS and PTEN gene mutations. Thus, PTEN gene-containing rNDV may be a promising candidate for pancreatic cancer treatment.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.