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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE152876 | GEO | 2020/11/16

REPOSITORIES: GEO

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Intravenous injection of oncolytic virus M1 awakes antitumor T cells and overcomes resistance to checkpoint blockade

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

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

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The multifaceted responses of human monocytes to IFN-gamma and IL-4 are not reducible to M1/M2 polarization of Macrophages

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