ArticleVirology journal2026
Reovirus resistance in tumors mediated by elevated ISG expression: overcoming therapeutic resistance via JAK/STAT pathway modulation.
Article in Virology journal, 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
backgroundOncolytic viruses such as reovirus hold significant promise for cancer therapy, but their efficacy varies across tumor types due to heterogeneous tumor cell sensitivity to reovirus. Elucidating the molecular mechanisms underlying reovirus resistance is therefore critical to improving therapeutic outcomes for resistant tumors.
methodsWe comprehensively assessed the oncolytic sensitivity of 12 diverse tumor cell lines to reovirus, followed by transcriptomic analysis of two ovarian cancer cell lines with divergent responses. Differentially expressed resistance-associated genes were verified, and the Janus kinase-signal transducer and activator of transcription (JAK-STAT) pathway was modulated using the type I interferon (IFN) receptor agonist RO8191 and JAK inhibitor ruxolitinib to evaluate impacts on reovirus replication and oncolysis. Additionally, patient-derived primary breast cancer cells were tested to explore cross-resistance mechanisms between chemotherapy and reovirus.
resultsTumor cells were stratified into three groups: high sensitivity (HS, cell viability ≤ 50%), moderate sensitivity (MS, 50-80%), and low sensitivity/resistance (LS, ≥ 80%). Transcriptomic analysis revealed higher baseline IFN-stimulated gene (ISG) expression in reovirus-resistant cells, with 170 ISGs upregulated in LS cells (including 28 interferon-related DNA damage resistance signature (IRDS) genes). ISG overexpression correlated with reovirus resistance: ruxolitinib-mediated JAK-STAT inhibition reduced ISGs and enhanced oncolysis, while pathway activation suppressed reovirus replication. Unphosphorylated ISGF3 (U-ISGF3) may drive IRDS-related ISG expression, contributing to cross-resistance to doxorubicin and reovirus.
conclusionsTumor cell resistance to reovirus is associated with elevated baseline expression of specific ISGs, potentially mediated by U-ISGF3-induced IRDS upregulation. These insights provide a foundation for optimizing reovirus therapy in resistant tumors.
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