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E-GEOD-46821

ABSTRACT: Prdm5 suppresses ApcMin-driven intestinal adenomas and regulates monoacylglycerol lipase expression

OTHER RELATED OMICS DATASETS IN: PRJNA202403

PROVIDER: E-GEOD-46821 | ExpressionAtlas | 2015-07-13

REPOSITORIES: ExpressionAtlas

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			Action	DRS
	E-GEOD-46821-analysis-methods.tsv	Tabular
	E-GEOD-46821-atlasExperimentSummary.Rdata	Rdata
	E-GEOD-46821-configuration.xml	Xml
	E-GEOD-46821-percentile-ranks.tsv	Tabular
	E-GEOD-46821.condensed-sdrf.tsv	Tabular

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Project description:Prdm5 suppresses ApcMin-driven intestinal adenomas and regulates monoacylglycerol lipase expression

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Prdm5 suppresses ApcMin-driven intestinal adenomas and regulates monoacylglycerol lipase expression

Project description:PRDM proteins are tissue specific transcription factors often deregulated in diseases, particularly in cancer where different members have been found to act as oncogenes or tumor suppressors. PRDM5 is a poorly characterized member of the PRDM family for which several studies have reported a high frequency of promoter hypermethylation in cancers of gastrointestinal origin. We report here the characterization of Prdm5 knockout mice in the context of intestinal carcinogenesis. We demonstrate that loss of Prdm5 increases the number of adenomas throughout the murine small intestine on an ApcMin background. By genome-wide ChIP-seq and transcriptome analyses we identify loci encoding proteins involved in metabolic processes as prominent PRDM5 targets and characterize monoacylglycerol lipase (Mgll) as a direct PRDM5 target in human colon cancer cells and in Prdm5 mutant mouse intestines. Moreover, we report the downregulation of PRDM5 protein expression in human colon neoplastic lesions. In summary, our data provide the first causal link between Prdm5 loss and intestinal carcinogenesis and uncover an extensive and novel PRDM5 target repertoire likely facilitating the tumor suppressive functions of PRDM5. Two experimental conditions: wt and ko mice for PRDM5. Each experimental condition was replicated three times. This submission represents transcriptome component of study.

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