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

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

PROVIDER: PRJNA555317 | ENA |

REPOSITORIES: ENA

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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

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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.

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Gene expression profiles of rat hypertrophic zone after treatment of CNP53 or U0126 [U0126]

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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.

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Transcriptome profile of HCT 116p53-/- and HCT 116p53-/- RPL3 KO during Actinomycin (Act D) treatment

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Expression data from colorectal cancer cell line HCT-116

Project description:We used microarrays to detail the global gene expression in cell line with or without M1 virus infection.

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Gene expression profile of human colorectal carcinoma HCT 116 cell line treated with imipramine

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Gene alterations by PPAR-gamma agonists in human colorectal adenocarcinoma HCT-116 cells

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Nonwoven-based gelatin/polycaprolactone membrane loaded with ERK inhibitor U0126 for treatment of tendon defects

Project description:Background: Tendon is a major component of musculoskeletal system connecting the muscles to the bone. Tendon injuries are very common orthopedics problems leading to impeded motion. Up to now, there still lacks effective treatments for tendon diseases. Methods: Tendon stem/progenitor cells (TSPCs) were isolated from the patellar tendons of SD rats. The expression levels of genes were evaluated by quantitative RT-PCR. Immunohistochemistry staining was performed to confirm the presence of tendon markers in tendon tissues. Bioinformatics analysis of data acquired by RNA-seq was used to find out the differentially expressed genes. Rat patellar tendon injury model was used to evaluate the effect of U0126 on tendon injury healing. Biomechanical testing was applied to evaluate the mechanical properties of newly formed tendon tissues. Results: In this study, we have shown that ERK inhibitor U0126 rather PD98059 could effectively increase the expression of tendon-related genes and promote the tenogenesis of TSPCs in vitro. To explore the underlying mechanisms, RNA sequencing was performed to identify the molecular difference between U0126-treated and control TSPCs. The result showed that GDF6 was significantly increased by U0126, which is an important factor of the TGFβ superfamily regulating tendon development and tenogenesis. In addition, NBM (nonwoven-based gelatin/polycaprolactone membrane) which mimics the native microenvironment of the tendon tissue was used as an acellular scaffold to carry U0126. The results demonstrated that when NBM was used in combination with U0126, tendon healing was significantly promoted with better histological staining outcomes and mechanical properties. Conclusion: Taken together, we have found U0126 promoted tenogenesis in TSPCs through activating GDF6, and NBM loaded with U0126 significantly promoted tendon defect healing, which provides a new treatment for tendon injury.

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