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

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

PROVIDER: PRJNA640682 | ENA |

REPOSITORIES: ENA

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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: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.

2020-11-16 | GSE152876 | 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

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

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

Oncolytic virus M1 functions as a bi-functional checkpoint inhibitor to enhance the antitumor activity of DC vaccine

Project description:Although promising, dendritic cell (DC) vaccines still provide limited clinical benefits, mainly due to the immunosuppressive tumor microenvironment (TME) and the lack of tumor-associated antigens (TAAs). Oncolytic viruses are considered to be an ideal strategy to overcome immunosuppression and expose TAAs, therefore they may work synergistically with DC vaccines. In this study, we demonstrated that oncolytic virus M1 (OVM) can enhance the antitumor effects of DC vaccine in a variety of syngeneic tumor mouse models by increasing the infiltration of CD8+ effector T cells in the TME. Mechanically, we identified that tumor cells offset the function of DC vaccines through the myeloid immune checkpoint SIRPα-CD47, while OVM can downregulate the expression of SIRPα and CD47 in DCs and tumor cells, respectively. Based on the fact that OVM upregulates the expression of PD-L1 in DCs, PD-L1 blockade was introduced with the combination of DC vaccines and OVM, resulting in a further potentiation of antitumor activity. Overall, we revealed that OVM can strengthen the antitumor efficacy of DC vaccines by targeting the immune checkpoint SIRPα-CD47 axis, which exerts dominant immunosuppressive effects on DC vaccines.

2023-09-01 | GSE222080 | GEO

Itaconate enhances oncolytic virotherapy via multitarget inhibition of antiviral and inflammatory pathways

Project description:4 octyl itaconate (4-OI) is a known anti-inflammatory chemical that activates Nrf2 signaling. Here, we are exploring the capacities of 4-OI to promote the spread of oncolytic Vesicular Stomatitis Virus (VSVd51M) in pLenti control kidney adenocarcinoma 786-O cell line and in Nrf2 knock out 786-O.

2023-06-15 | GSE232509 | GEO

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

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

| PRJNA555317 | ENA

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

Resistance of primary ovarian cancer cells to oncolytic adenoviruses

Project description:This SuperSeries is composed of the following subset Series: GSE15350: Resistance of primary ovarian cancer cells to oncolytic adenoviruses part1 of 2 GSE15351: Resistance of primary ovarian cancer cells to oncolytic adenoviruses part2 of 2 Refer to individual Series

2009-04-01 | E-GEOD-15473 | biostudies-arrayexpress

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

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

| PRJNA639448 | ENA