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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.

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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

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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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MYC induces immunotherapy and interferon-γ resistance through downregulation of JAK2

Project description:Immunotherapy revolutionized the treatment of advanced melanoma. As the pathways mediating resistance to immunotherapy are largely unknown, we conducted transcriptome profiling of pre-immunotherapy tumor biopsies from melanoma patients that received PD-1 blockade (n=36) or adoptive cell therapy with tumor infiltrating lymphocytes (n=37). We identified two melanoma-intrinsic mutually exclusive gene programs, which are controlled by interferon-γ and MYC, and determine immunotherapy outcome. MYC-overexpressing melanoma cells exhibited lower interferon-γ responsiveness, which was linked with JAK2 downregulation. Luciferase activity assays under the control of JAK2 promoter demonstrated reduced activity in MYC-overexpressing cells, which was reversible upon mutagenesis of MYC E-box binding sites in the JAK2 promoter. Moreover, silencing of MYC or its co-factor MAX with siRNA increased JAK2 expression and interferon-γ responsiveness of melanomas, while concomitantly enhancing the effector functions of T-cells co-incubated with MYC-overexpressing cells. Thus, we propose that MYC plays a pivotal role in immunotherapy resistance through downregulation of JAK2.

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