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Gene expression profiles of murine melanomas after treatment with STING agonist ADU-S100 [II]

ABSTRACT: Two murine melanoma models (B16 and BPR) were treated with PBS or STING agonist ADU-S100 in vivo. Dose 1 was administered intratumorally on day 10, and a second dose was given on day 14. Tumors were collected 6 hours after the second dose and RNA was isolated. RNA was run on the Nanostring mouse PanCancer Immune Profiling Panel.

ORGANISM(S): Mus musculus

PROVIDER: GSE249295 | GEO | 2023/12/09

REPOSITORIES: GEO

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Project description:Purpose: Next-generation sequencing (NGS)-derived transcriptome profiling (RNA-seq) is a powerful tool for analysing cellular pathways involved in treatment responses. In this study, RNA-seq was used to perform differential gene expression (DEG) and gene ontology (GO) analyses in prostate tumors treated with different immunotherapies and their combination. This was in order to investigate which pathways are activated and mediate the therapeutic effect. Methods: Mice with TRAMP-C2 subcutaneous prostate tumors were treated with either HBSS (control) or cyto-IL-15 or the STING agonist ADU-S100 or combination of ADU-S100 and cyto-IL-15. At day 6, tumors were removed and RNA was harvested to be used for RNA sequencing with Illumina NovaSeq. Using DESeq2, a comparison of gene expression between the treatment cohorts was performed and the Wald test was used to generate p-values and Log2 fold changes. GO analysis was performed on the statistically significant genes by implementing GeneSCF software using Fisher exact test. The mgi GO list was used to cluster the set of genes based on their biological process. Results: DEG analysis shown that more than 1,000 genes were differentially expressed in tumors 6 days after treatment with ADU-S100 or its combination with cyto-IL-15 (1,040 genes for ADU-S100 compared to control; 1,141 genes for combination compared to control). Most of the differentially expressed genes were upregulated (>70% in both comparisons). cyto-IL-15 led to differential expression of 96 genes compared to control. Differential expressed genes included Cxcl11 involved in immune cell recruitment and activation, and genes encoding granzymes a and b, which are proteases released by cytotoxic T cells and natural killer (NK) cells to kill cancer cells. In the control versus ADU-S100 or combination comparisons, GO analysis revealed that the majority of genes were involved in processes such as cellular responses to interferon-γ and β, complement activation, innate immune response, phagocytosis, and B cell signalling and activation. Conclusions: This study provides valuable insights in differential expression and activation of genes and cellular pathways involved in eliciting responses to immunotherapies in mouse prostate tumors. Using NSG and more specifically RNAseq-based transcriptome characterization, a detailed quantitative and qualitative analysis on how novel therapies exert their efficacy in tumors can be achieved and uncover the specific biological processes and functions contributing to the anti-tumor effects.

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Gene expression profiles of murine melanomas after treatment with STING agonist ADU-S100 [II]

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