Lonidamine enhances the oncolytic effect of M1 virus through inhibiting antiviral immune response and potentiating ER stress mediated apoptosis

Gene set enhancement analysis (GSEA) revealed that M1 treatment upregulates glycolysis and hypoxia pathway in hallmark gene sets. GSEA revealed that Lonidamine strongly inhibited the IFN-α and IFN-β response pathways after M1 virus infection. GSEA showed that gene sets in unfolded protein response, response to endoplasmic reticulum stress, intrinsic apoptotic signaling pathway were significantly upregulated by Lonidamine plus M1 treatment. HCT 116 tumor cells were treated with control, M1 (MOI=1 pfu/cell), Lonidamine [cp531] (50 μM) or M1 (MOI=1 pfu/cell) plus Lonidamine (50 μM) for 24 hours. Total RNA was extracted from 1×106 cells with TRIzol Reagent (Thermo Fisher Scientific) and was sent for RNA sequencing >>>Submitter states that all raw files were lost<<<