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Early life microbiota exposure restricts myeloid-derived suppressor cell driven colonic tumorigenesis

ABSTRACT: Early life microbiota exposure restricts myeloid-derived suppressor cell driven colonic tumorigenesis

PROVIDER: PRJEB30606 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR3039980.fastq.gz	Fastqsanger.gz
	ERR3039990.fastq.gz	Fastqsanger.gz
	ERR3039981.fastq.gz	Fastqsanger.gz
	ERR3039991.fastq.gz	Fastqsanger.gz
	ERR3039982.fastq.gz	Fastqsanger.gz

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Early life microbiota exposure restricts myeloid-derived suppressor cell driven colonic tumorigenesis

Project description:Early life microbiota exposure restricts myeloid-derived suppressor cell driven colonic tumorigenesis

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Early-Life Microbiota Exposure Restricts Myeloid-Derived Suppressor Cell-Driven Colonic Tumorigenesis.

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FOXO3 Deficiency in Neutrophils Drives Colonic Inflammation and Tumorigenesis

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FOXO3 Deficiency in Neutrophils Drives Colonic Inflammation and Tumorigenesis

Project description:FOXO3 Deficiency in Neutrophils Drives Colonic Inflammation and Tumorigenesis

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FOXO3 expression in macrophages is lowered by high fat diet and regulates colonic inflammation and tumorigenesis

Project description:Obesity, characterized by augmented inflammation and tumorigenesis, is linked to genetic predispositions, such as FOXO3 polymorphisms. As obesity is associated with aberrant macrophages infiltrating different tissue including the colon, we aimed to identify FOXO3-dependent transcriptomic changes in macrophages that drive obesity-mediated colonic inflammation and tumorigenesis. We found that in mouse colons, high-fat-diet-(HFD)-obesity led to diminished FOXO3 levels and increased macrophages. Transcriptomic analysis of mouse peritoneal FOXO3-deficient macrophages showed significant differentially expressed genes (DEGs; FDR<0.05) similar to HFD-obese colon. These DEGs related pathways, linked to mouse colonic inflammation and tumorigenesis, were similar to those in inflammatory bowel disease (IBD) and human colon cancer. Additionally, we identified a specific transcriptional signature for the macrophage-FOXO3 axis (MAC-FOXO382), which separated the transcriptome of affected tissue from control in both IBD (p=5.2E-08) and colon cancer (p=1.9E-11), revealing its significance in human colonic pathobiologies. Further, we identified (heatmap) and validated (qPCR) DEGs specific to FOXO3-deficient macrophages with established roles both in IBD and colon cancer (IL-1B, CXCR2, S100A8, S100A9, and TREM1) and those with unexamined roles in these colonic pathobiologies (STRA6, SERPINH1, LAMB1, NFE2L3, OLR1, DNAJC28 and VSIG10). These findings establish an important understanding of how HFD-obesity and related metabolites promote colonic pathobiologies.

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Project description:Neuroblastoma is a pediatric cancer of the sympathetic nervous system. MYCN amplification is a key indicator of poor prognosis for the disease, however, mechanisms by which MYCN promotes neuroblastoma tumorigenesis are not fully understood. In this study, we analyzed global miRNA and mRNA expression profiles of tissues at different stages of tumorigenesis from TH-MYCN transgenic mice, a model of MYCN-driven neuroblastoma. Based on a Bayesian learning network model in which we compared pre-tumor ganglia from TH-MYCN+/+ mice to age-matched wild-type controls, we devised a predicted miRNA-mRNA interaction network. Among the miRNA-mRNA interactions operating during human neuroblastoma tumorigenesis, we identified that miR-204 is a tumor suppressor miRNA that inhibits a subnetwork of oncogenes strongly associated with MYCN-amplified neuroblastoma and poor patient outcome. Accordingly, we found that MYCN was bound to the miR-204 promoter and repressed miR-204 transcription, while in contrast, miR-204 directly bound MYCN mRNA and repressed MYCN expression. In support of a tumor suppressor role, miR-204 overexpression significantly inhibited neuroblastoma cell proliferation in vitro and tumorigenesis in vivo. Together these findings identify novel tumorigenic miRNA gene networks and miR-204 as a tumor suppressor that regulates MYCN expression in neuroblastoma tumorigenesis.

2018-06-01 | GSE100658 | GEO

BRG1 attenuates colonic inflammation and tumorigenesis through autophagy-dependent oxidative stress sequestration

Project description:BRG1 attenuates colonic inflammation and tumorigenesis through autophagy-dependent oxidative stress sequestration

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Inhibition of pluripotency networks by the Rb tumor suppressor restricts reprogramming and tumorigenesis.

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