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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

Project description:Gene set enrichment analysis (GSEA) revealed that upon M1 treatment, apoptotic and inflammation associated genes were largely upregulated, suggesting that M1 killed tumor cells and triggered inflammatory response. The GSEA also revealed that DNA repair pathway was down-regulated in M1 treated tumors, which is consistent with our previous finding that M1 induces DNA damage and then leads to tumor cells apoptosis. Additionally, gene sets marked the release of immune-boosting cytokines such as interferon (IFN)-α, IFN-γand tumor necrosis factor (TNF)-α were deployed in M1 treated tumors, providing potential pro-inflammatory signals to generate antitumor immunity. All the results above demonstrate that M1 induces ICD and shapes TME to an inflammatory state.

2020-12-21 | GSE152451 | GEO

DNA-PK inhibition synergizes with oncolytic virus M1 by inhibiting antiviral response and potentiating DNA damage.

Project description: Not available

| S-EPMC6194050 | biostudies-literature

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

| PRJNA640682 | ENA

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

Project description:Macrophages are known to be polarized into inflammatory (M1) and immunoregulatory (M2) cells when they are stimulated by agonists such as IFN-gamma and IL-4, respectively. If circulating monocytes may be polarized in response to T cell signals is often misguidedly deduced from macrophage results. Here the transcriptional responses of human CD14+ monocytes to IFN-gamma and IL-4 were analyzed using whole genome microarrays. A principal component analysis and hierarchical clustering showed that monocyte and macrophage responses were distinct. Monocytes stimulated with IFN-gamma and IL-4 for 6 hours exhibited some features of macrophage polarization. Indeed, when 80 genes considered as M1 and M2 genes were analyzed, we found that M1 genes were modulated in response to IFN-gamma and that M2 genes were modulated in response to IL-4. The M1 polarization of monocytes was transient because only M2 genes were modulated when monocytes were stimulated with IFN-gamma and IL-4 for 18 hours. However, the activation of monocytes by IFN-gamma and IL-4 could not be reduced to M1/M2 polarization status. Indeed, monocytes exhibited early specific signatures composed of 46 and 39 up-regulated genes in response to IFN-gamma and IL-4, respectively, and a late signature common to both molecules that consisted of 57 up-regulated genes. Taken together, these results demonstrated the extreme plasticity of human monocytes and suggested the existence of a core transcriptional termination program. Using early and late signatures might be pertinent to investigate monocyte activation in inflammatory or infectious diseases. Monocytes were stimulated with IFN-gamma (20ng/mL) or IL-4 (20ng/mL) for 6 and 18 hours or culture for 6 and 18 hours without agonist (Unstimulated samples). Monocytes-derived-macrophages (MDM) stimulated with IFN-gamma and IL-4 for 18 hours were used as controls. Each microarray is derived from a single biological sample.

2013-03-15 | E-GEOD-36537 | biostudies-arrayexpress

Expression profiles of M1-polarized RAW264.7 cells [RAW_M1vsM0_RNA-seq]

Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to evaluate the gene expression of M1-polarized RAW264.7 cells compared with M0 RAW264.7 cells. Methods: RAW264.7 cells were polarized toward M1 using LPS and IFN-γ. M0 RAW264.7 cells were maintained in culture without LPS and IFN-γ. Total RNA of M1 and M0 RAW264.7 cells was extracted. RAW264.7 cells RNA profiles were generated by deep sequencing for two groups (M1 versus M0 RAW264.7 cells) with three samples each. Results: There were significant differences between M1 and M0 RAW264.7 cells. Conclusions: Polarization of RAW264.7 cells from M0 to M1 induces various changes at the transcription level.

2024-03-31 | GSE183077 | GEO

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

2013-03-15 | GSE36537 | GEO

Expression data from colorectal carcinoma HCT-15 treated with oncolytic virus M1 and U0126

Project description:Virus infection is a kind of immune stimulation, we previously found that inhibition of Ras signaling by U0126 supress the infection of M1 virus, thus we predicted that U0126 might increase the antiviral effect, ultimately inhibit the replication of M1 virus. We plan to figure it out from the expression array data. We used microarry data to detail the expression of immune factors regulated by oncolytic virus M1 and U0126.

2019-07-19 | GSE134487 | GEO

Expression data from HCT 116 colorectal cancer cells treated with oncolytic virus M1

Project description:Virus infection is a kind of immune stimulation, except anti-viral factors, virus also induce tumor cells to secret cytokines which act on neighboring cells. Figuring out the exact cytokines upregulated by M1 virus is of great significance. We used microarry data to detail the expression of cytokines, chemokines and Inflammasomes regulated by oncolytic virus M1.

2016-12-27 | GSE92918 | GEO

IFN-γ selectively suppresses a subset of TLR4-activated genes and enhancers to potentiate M1-like macrophage polarization [RNA-seq]

Project description:Complete polarization of macrophages towards an M1-like proinflammatory and antimicrobial state requires combined action of IFN-γ and LPS. Synergistic activation of canonical inflammatory NF-κB target genes by IFN-γ and LPS is well appreciated, but less is known about whether IFN-γ negatively regulates components of the LPS response, and how this affects polarization. A combined transcriptomic and epigenomic approach revealed that IFN-γ selectively abrogates LPS-induced feedback and select metabolic pathways by suppressing TLR4-mediated activation of gene enhancers. In contrast to superinduction of inflammatory genes via enhancers that harbor IRF sequences and bind STAT1, IFN-γ-mediated repression targeted enhancers with STAT sequences that bound STAT3. TLR4-activated IFN-γ-suppressed enhancers comprised two subsets distinguished by differential regulation of histone acetylation and recruitment of STAT3, CDK8 and cohesin, and were functionally inactivated by IFN-γ. These findings reveal that IFN-γ suppresses feedback inhibitory and metabolic components of the TLR response to achieve full M1 polarization, and provide insights into mechanisms by which IFN-γ selectively inhibits TLR4-induced transcription.

2019-06-12 | GSE120944 | GEO

IFN-γ selectively suppresses a subset of TLR4-activated genes and enhancers to potentiate M1-like macrophage polarization [ChIP-seq]

2019-06-12 | GSE120943 | GEO

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