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E-MTAB-7123

ABSTRACT: Transcription profiling of B16V mouse melanoma cells after BAG6 knockout to study impacts on extracellular vesicle mRNA cargo

PROVIDER: E-MTAB-7123 | ExpressionAtlas | 2019-01-16

REPOSITORIES: ExpressionAtlas

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Dataset's files

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			Action	DRS
	E-MTAB-7123-analysis-methods.tsv	Tabular
	E-MTAB-7123-analytics.tsv	Tabular
	E-MTAB-7123-atlasExperimentSummary.Rdata	Rdata
	E-MTAB-7123-configuration.xml	Xml
	E-MTAB-7123-g2_g1-mvaPlot.png	Other

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Project description:Extracellular vesicles (EVs) secreted by tumor cells are able to establish a pre-metastatic niche in distant organs, or on the contrary, exert anti-tumor activity. The mechanisms directing distinct EV functions are unknown. Using the B-16V transplantation mouse melanoma model we demonstrate that EVs from B-16V cells mobilize Ly6Clow patrolling monocytes and inhibit lung metastasis. Mechanistically, the formation of anti-tumor-EVs was dependent on the chaperone BAG6 and the acetylation of p53 by the BAG6/CBP/p300-acetylase complex, followed by the recruitment of components of the endosomal sorting complexes required for transport (ESCRT) via a P(S/T)AP double motif of BAG6. By contrast, deficiency of BAG6 led to the release of a distinct vesicle subtype with pro-tumorigenic activity, which recruited neutrophils to the pre-metastatic niche. In humans, BAG6 expression decreases in late-stage melanoma patients, correlating with an increase of the mRNA for the metastasis driver alpha-catulin in EVs, as observed in BAG6-deficient mouse EVs. We conclude that the BAG6/CBP/p300-p53 axis is a key pathway directing EV-formation and function.

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