Reovirus resistance in tumors mediated by elevated ISG expression: overcoming therapeutic resistance via JAK/STAT pathway modulation

Key Points

• Investigate how elevated ISG expression contributes to reovirus resistance in tumor cells.
• Analysis of baseline ISG expression levels in tumor cells
• Examination of U-ISGF3-induced IRDS upregulation
• Assessment of the JAK/STAT pathway's role in therapeutic response
• High ISG expression levels correlate with increased resistance to reovirus
• U-ISGF3 was identified as a key mediator of IRDS upregulation
• Modulating the JAK/STAT pathway may enhance reovirus therapy efficacy