ArticleThe Malaysian journal of medical sciences : MJMS2026
Genetic Regulation of ERK1/2-c-Fos Signalling Pathway in Newcastle Disease Virus-Induced Apoptosis of Human Pancreatic Cancer Stem Cells.
Article in The Malaysian journal of medical sciences : MJMS, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive cancer with a five-year survival of approximately 6% that is largely driven by cancer stem cells (CSCs), which promote resistance, metastasis, and recurrence. Mutations in the Ki-ras2 Kirsten rat sarcoma viral oncogene homolog (K-RAS) are common in human PDAC and activate the rat sarcoma (RAS) pathway, thus supporting tumour growth, maintenance, and metastasis. Newcastle Disease Virus (NDV) is a tumour-selective oncolytic virus with a strong safety profile that targets cancer cells and therapy-resistant CSCs, thereby highlighting its potential as an anticancer virotherapy. This study examines NDV AF2240's ability to target CSCs through RAS pathway modulation and apoptosis induction. Methods: NDV AF2240 was titrated by hemagglutination (HA) and plaque assays using Vero cells. CSCs were isolated from Panc-1 cells and confirmed by sphere-formation, flow cytometry, and RT-qPCR for CD24, CD44, and EpCAM/ESA. Cells were infected at multiplicities of infection (MOIs) of 0.1, 0.5, 1, and 10 for 24-72 h. Cytopathic effects were assessed with an MTS assay, and apoptosis was assessed by the expression of Caspase-3, -8, and -9, Bax, and Bcl- 2. NDV reduced CSC viability in a time- and dose-dependent manner, with significant declines at 24-48 and 72 h ( Results: NDV AF2240 induced effective cytopathic effects in PDAC stem cells, downregulating the K-RAS effectors ERK1/2 and C-FOS, triggering apoptosis, and reducing the viability of PDAC CSCs in vitro. Conclusion: These findings highlight NDV's potential as an oncolytic agent against PDAC stem cells via the modulation of ERK1/2 and C-FOS, thus supporting its therapeutic development.
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