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Platinoid drugs augment immunotherapy via histone acetylation of MHCI machinery genes [CCO19-MC]

ABSTRACT: Platinoid drugs augment immunotherapy via histone acetylation of MHCI machinery genes [CCO19-MC]

PROVIDER: PRJNA521467 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8550200.fastq.gz	Fastqsanger.gz
	SRR8550201.fastq.gz	Fastqsanger.gz
	SRR8550202.fastq.gz	Fastqsanger.gz
	SRR8550203.fastq.gz	Fastqsanger.gz
	SRR8550204.fastq.gz	Fastqsanger.gz

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Platinoid drugs augment immunotherapy via histone acetylation of MHCI machinery genes

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Platinoid drugs augment immunotherapy via histone acetylation of MHCI machinery genes [AT_MC]

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Platinoid drugs augment immunotherapy via histone acetylation of MHCI machinery genes [TRAMP]

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Platinoid drugs augment immunotherapy via histone acetylation of MHCI machinery genes [Myc_CaP]

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Platinoid drugs augment immunotherapy via histone acetylation of MHCI machinery genes [CCO19-MC]

Project description:Here we show that low dose Oxali, and to a lesser extent other platinoids, can uniquely activate the transcriptional program that controls MHCI antigen processing and presentation. Activation of this program correlates with induction of histone acetylation and enhanced chromatin accessibility. Oxaliplatin also induces NF-kB dependent IFNg receptor 2 (IFNgR2) thereby augmenting the tumor response to exogenous IFNg produced by reinvigorated effector CD8+ T cells.

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Platinoid drugs augment immunotherapy via histone acetylation of MHCI machinery genes [Myc_CaP]

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Platinoid drugs augment immunotherapy via histone acetylation of MHCI machinery genes [AT_MC]

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Platinoid drugs augment immunotherapy via histone acetylation of MHCI machinery genes [TRAMP]

2021-02-01 | GSE126273 | GEO

Platinoid drugs augment immunotherapy via histone acetylation of MHCI machinery genes

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-02-01 | GSE126288 | GEO

Comparison of the MC-LR and MC-RR effects on Caco-2 cells

Project description:Microcystins (MCs) are cyclic hepatotoxins produced worldwide by various species of cyanobacteria. Their structure includes two variable amino acids (AAs) and most of the studies focused on the most toxic variant: the microcystin LR (MC-LR). However, more than 80 MC variants have been described to date. Despite ingestion being the major pathway of human exposure, few in vivo studies have demonstrated macroscopic effects on the gastro-intestinal tract, but no data are available on the affected pathways by several variants on intestinal cells. Here, using a non-selective method, we investigated for the first time the effect of MC-RR and MC-LR on the human intestinal cell line Caco-2 and compared their response at the pangenomic scale. The cells were incubated for 4 hrs or 24 hrs with the same range of sub-lethal concentrations of MC-RR or MC-LR. Low effects were observed for both variants after a short-term exposure. On the contrary, dose-dependent modulations of the genes transcription levels were noticed with MC-RR and MC-LR after 24 hrs. Furthermore, the genomic profiles induced by both variants were similar suggesting a common toxicity mechanism but with higher modulation following MC-LR than MC-RR exposure. However, the functional annotation revealed major differences between the variants effects. Indeed, the well-known MC-LR affected mainly two pathways, the oxidative stress response and the cell cycle regulation, which did not elicit significant alteration following MC-RR exposure. This work is the first comparative description of the MC-LR and MC-RR effects on a human intestinal cell model. It allowed us to suggest differences in the mechanism of toxicity for MC-RR and MC-LR. These results illustrate that the toxicity of MC variants remains a key point for risk assessment.

2012-12-31 | GSE29861 | GEO

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