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Melanoma dedifferentiation induced by interferon-gamma epigenetic remodeling in response to anti-PD-1 therapy

ABSTRACT: Melanoma dedifferentiation induced by interferon-gamma epigenetic remodeling in response to anti-PD-1 therapy

PROVIDER: PRJNA640390 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12046225.fastq.gz	Fastqsanger.gz
	SRR12046226.fastq.gz	Fastqsanger.gz
	SRR12046227.fastq.gz	Fastqsanger.gz
	SRR12046228.fastq.gz	Fastqsanger.gz
	SRR12046229.fastq.gz	Fastqsanger.gz

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Melanoma dedifferentiation induced by interferon-gamma epigenetic remodeling in response to anti-PD-1 therapy

Project description:Melanoma dedifferentiation has been reported as a state of cellular resistance to targeted therapies and immunotherapies as cancer cells revert to a more primitive cellular phenotype. Here we show that, counterintuitively, the biopsies of patient tumors that respond to anti-programmed cell death receptor 1 (PD-1) therapy decreased expression of melanocytic markers and increased neural crest markers, suggesting treatment-induced dedifferentiation. When modeling the effects in vitro, we documented that melanoma cell lines that were originally melanocytic differentiated underwent a process of neural crest dedifferentiation when continuously exposed to interferon gamma (IFNγ), through a global chromatin landscape changes leading to enrichment in specific hyperaccessible chromatin regions. The IFNγ-induced dedifferentiation signature corresponded with improved outcomes in patients with melanoma, challenging the notion that neural crest dedifferentiation is entirely an adverse phenotype.

2021-05-10 | GSE152755 | GEO

Melanoma dedifferentiation induced by interferon-gamma epigenetic remodeling in response to anti-PD-1 therapy

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Melanoma dedifferentiation induced by interferon-gamma epigenetic remodeling in response to anti-PD-1 therapy

Project description:Melanoma dedifferentiation induced by interferon-gamma epigenetic remodeling in response to anti-PD-1 therapy

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Interferon receptor signaling pathways regulating PD-L1 and PD-L2 expression

Project description:We studied the molecules involved in downstream signaling induced by interferons to regulate PD- L1 and PD-L2 expression using a shRNA screen, Western blot, mRNAexpression profiling, promoter truncation analysis and chromatin immunoprecipitation.These studies revealed that the interferon gamma-JAK1/2-STAT1-IRF1 axis primarily regulates PD-L1 expression, with IRF1 binding to its promoter. PD-L2 responded equally to interferon beta and gamma, and shared regulation through IRF1 and alsoSTAT3, which bind to the PD-L2 promoter. Analysis of biopsies from patients with melanoma confirmed interferon signature enrichment and upregulation of gene targets for STAT1/2/3 and IRF1 in anti-PD-1 responding tumors. Therefore, these studies map the signaling pathway of interferon-inducible PD-1 ligand expression

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Interferon Gamma signaling triggers dysplastic alveolar remodeling during respiratory viral infection

Project description:Interferon Gamma signaling triggers dysplastic alveolar remodeling during respiratory viral infection

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Interferon Gamma signaling triggers dysplastic alveolar remodeling during respiratory viral infection

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Conserved interferon-gamma signaling and decreased immune exclusion programs in responses to immune checkpoint blockade therapy

Project description:We analyzed baseline and on-therapy tumor biopsies from 101 patients with advanced melanoma treated with nivolumab (anti-PD-1) alone or combined with ipilimumab (anti-CTLA-4). Analysis of whole transcriptome data showed that T cell infiltration and interferon-gamma signaling signatures corresponded most highly with clinical response to therapy, with a reciprocal decrease in cell cycle and WNT signaling pathways in responding biopsies. Clinical outcome differences were likely not due to differential melanoma cell responses to interferon-gamma, as 57 human melanoma cell lines exposed in vitro to this cytokine showed a conserved interferon-gamma transcriptome response unless they had mutations that precluded signaling from the interferon-gamma receptor. Therefore, the magnitude of the antitumor T cell response and the corresponding downstream interferon-gamma signaling are the main drivers of clinical response or resistance to immune checkpoint blockade therapy.

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Project description:Monocyte derived macrophages were exposed to arachidonic acid, interferon beta, or interferon gamma

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Transcription profiling of Toxoplasma-infected human fibroblasts treated with human recombinant interferon gamma

Project description:Human fibroblasts were infected or not with Toxoplasma gondii (Pru strain) for 18 h at a nominal MOI of 3. Cells were subsequently treated with human recombinant interferon gamma (0.5 ng/ml = 30 pM) for 0, 2, 4 and 8 h before RNA was harvested for cDNA microarray experiments. Uninfected samples were named N0, N2, N4 and N8 (i.e., N2 indicated uninfected cells treated with interferon gamma for 2 h); infected samples were named P0, P2, P4 and P8. Duplicate cultures were analyzed for each condition (indicated as "a" and "b"). The reference channel (ch1, green) contained Universal Human Reference RNA. Using a genome-wide microarray analysis we show here a complete dysregulation of interferon-gamma-inducible gene expression in human fibroblasts infected with Toxoplasma. Notably, 46 of the 127 interferon-gamma-responsive genes were induced and 19 were suppressed in infected cells before they were exposed to interferon gamma, indicating that other stimuli produced during infection may also regulate these genes. Following interferon-gamma treatment, none of the 127 interferon-gamma-responsive genes could be significantly induced in infected cells.

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