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Bulk RNA-seq analysis of molecular characteristics induced by Aoah over-expression in MYC-Luc spontaneous hepatocellular carcinoma tumors

ABSTRACT: Bulk RNA-seq analysis of molecular characteristics induced by Aoah over-expression in MYC-Luc spontaneous hepatocellular carcinoma tumors

PROVIDER: PRJNA1234191 | ENA |

REPOSITORIES: ENA

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Bulk RNA-seq analysis of molecular characteristics induced by Aoah over-expression in MYC-Luc spontaneous hepatocellular carcinoma tumors

Project description:Secreted proteins are central mediators of intercellular communications and can serve as therapeutic targets in diverse diseases. The ~1903 human genes encoding secreted proteins are difficult to study through common genetic approaches. To address this hurdle and, more generally, to discover cancer therapeutics, we developed the Cancer Immunology Data Engine (CIDE, https://cide.ccr.cancer.gov), which incorporates 90 omics datasets spanning 8575 tumor profiles with immunotherapy outcomes from 17 solid tumor types. CIDE systematically identifies all genes associated with immunotherapy outcomes. Then, we focused on secreted proteins prioritized by CIDE without known cancer roles and validated regulatory effects on immune checkpoint blockade for AOAH, CR1L, COLQ, and ADAMTS7 in mouse models. The top hit, AOAH (Acyloxyacyl Hydrolase), potentiates immunotherapies in multiple tumor models by sensitizing T-cell receptors to weak antigens and protecting dendritic cells through depleting immunosuppressive arachidonoyl phosphatidylcholines and oxidized derivatives.

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Single-cell analysis of immune cell characteristics induced by Aoah over-expression in MYC-Luc spontaneous hepatocellular carcinoma tumors

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Single-cell analysis of immune cell characteristics induced by Aoah over-expression in MYC-Luc spontaneous hepatocellular carcinoma tumors

Project description:Single-cell analysis of immune cell characteristics induced by Aoah over-expression in MYC-Luc spontaneous hepatocellular carcinoma tumors

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Bulk RNA-seq analysis of molecular characteristics induced by Aoah over-expression in B16 subcutaneous implanted tumors

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Genome-wide anyalysis of gene expression during prolonged endotoxin tolerance in Aoah -/- mice

Project description:Analysis of gene expression in explanted peritoneal macrophages from Aoah -/- and Aoah +/+ mice treated with LPS 21 days prior to harvest. Explanted peritoneal machrophages were challenged with LPS or control (PBS). The study seeks to characterize global gene expression in the state of prolonged LPS tolerance induced in mice lacking the LPS-inactivating enzyme Aoah. Groups of 9 C57BL/6 Aoah+/+ or Aoah-/- mice were given i.p. injections of 10 µg E. coli LPS/mouse. Twenty-one days later (when Aoah-/- mice remain tolerant and Aoah+/+ mice have recovered), peritoneal macrophages were harvested and the yields from three mice were pooled to form 3 samples per group (i.e., three samples of Aoah+/+ and Aoah-/- mice, with each sample comprised of peritoneal macrophages from 3 mice). Next day, cells were challenged with LPS or PBS and whole RNA was isolated 2 hours later and used for microarray experiments.

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RNA Expression Data from IL-15-/- and IL-15+/+ TAX-LUC Mouse Tumors

Project description:IL-15 is recognized as a promising candidate for tumor immunotherapy and has been described as both a promoter of cancer and a promoter of anti-cancer immunity. IL-15 was discovered in cells transformed by HTLV-1, the etiologic agent of adult T cell leukemia / lymphoma (ATL) and the human retrovirus that carries the Tax oncogene. We have developed the TAX-LUC mouse model of ATL in which Tax expression drives both malignant transformation and luciferase expression, enabling non-invasive imaging of tumorigenesis in real time. To identify the role of IL-15 in spontaneous development of lymphoma in vivo, an IL-15-/- TAX-LUC strain was developed and examined. The absence of IL-15 resulted in aggressive tumor growth and accelerated mortality and demonstrated that IL-15 was not required for Tax-mediated lymphoma but was essential for anti-tumor immunity. Further analysis revealed a unique transcriptional profile in tumor cells that arise in the absence of IL-15 that included a significant increase in the expression of IL-1α and IL-1α-regulated cytokines. Moreover, anti-IL-1α antibodies and an IL-1 receptor antagonist (Anakinra) were used to interrogate the potential of IL-1α targeted therapies in this model. Taken together, these findings identify IL-15 and IL-1α as therapeutic targets in lymphoma. We used microarrays to compare the gene expression profile of tumors in IL-15-/- TAX-LUC mice to IL-15+/+ TAX-LUC mice

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