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CD8+ T cell responsiveness to anti-PD-1 is epigenetically regulated by Suv39h1 in melanomas [ATAC-seq]

ABSTRACT: Purpose: We show that genetic ablation or pharmacological inhibition of H3K9-methyl transferase Suv39h1 delays tumor growth and potentiates tumor rejection by anti-PD-1.

ORGANISM(S): Mus musculus

PROVIDER: GSE198421 | GEO | 2022/03/14

REPOSITORIES: GEO

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CD8+ T cell responsiveness to anti-PD-1 is epigenetically regulated by Suv39h1 in melanomas [scRNA-seq]

Project description:Purpose: We show that genetic ablation or pharmacological inhibition of H3K9-methyl transferase Suv39h1 delays tumor growth and potentiates tumor rejection by anti-PD-1.

2022-03-14 | GSE198422 | GEO

CD8+T cell responsiveness to anti-PD-1 is epigenetically regulated by Suv39h1 in melanomas.

Project description:Tumor-infiltrating CD8 + T cells progressively lose functionality and fail to reject tumors. The underlying mechanism and re-programing induced by checkpoint blockers are incompletely understood. We show here that genetic ablation or pharmacological inhibition of histone lysine methyltransferase Suv39h1 delays tumor growth and potentiates tumor rejection by anti-PD-1. In the absence of Suv39h1, anti-PD-1 induces alternative activation pathways allowing survival and differentiation of IFNγ and Granzyme B producing effector cells that express negative checkpoint molecules, but do not reach final exhaustion. Their transcriptional program correlates with that of melanoma patients responding to immune-checkpoint blockade and identifies the emergence of cytolytic-effector tumor-infiltrating lymphocytes as a biomarker of clinical response. Anti-PD-1 favors chromatin opening in loci linked to T-cell activation, memory and pluripotency, but in the absence of Suv39h1, cells acquire accessibility in cytolytic effector loci. Overall, Suv39h1 inhibition enhances anti-tumor immune responses, alone or combined with anti-PD-1, suggesting that Suv39h1 is an "epigenetic checkpoint" for tumor immunity.

| S-EPMC9243005 | biostudies-literature

CD8+ T cell responsiveness to anti-PD-1 is epigenetically regulated by Suv39h1 in melanomas

Project description:CD8+ T cell responsiveness to anti-PD-1 is epigenetically regulated by Suv39h1 in melanomas

| PRJNA815051 | ENA

CD8+ T cell responsiveness to anti-PD-1 is epigenetically regulated by Suv39h1 in melanomas

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

2022-03-14 | GSE198423 | GEO

CD8+ T cell responsiveness to anti-PD-1 is epigenetically regulated by Suv39h1 in melanomas [scRNA-seq]

Project description:CD8+ T cell responsiveness to anti-PD-1 is epigenetically regulated by Suv39h1 in melanomas [scRNA-seq]

| PRJNA815054 | ENA

CD8+ T cell responsiveness to anti-PD-1 is epigenetically regulated by Suv39h1 in melanomas [ATAC-seq]

Project description:CD8+ T cell responsiveness to anti-PD-1 is epigenetically regulated by Suv39h1 in melanomas [ATAC-seq]

| PRJNA815055 | ENA

SUV39H1 Maintains Cancer Stem Cells in Glioblastoma [RNA-seq]

Project description:Glioblastoma (GBM) is the deadliest brain cancer, driven in part by GBM stem cells (GSCs) that contribute to therapeutic resistance and tumor recurrence. Effective targeting and elimination of GSCs hold promise for preventing GBM recurrence and achieving potential cures. In this study, we explored the role of the epigenetic regulator SUV39H1 in GSC maintenance and GBM progression. We observed that SUV39H1 is upregulated in GBM samples compared to normal brain tissues. Single-cell RNA-seq data indicated that SUV39H1 is preferentially expressed in GSCs relative to non-stem GBM cells, possibly due to super-enhancer-mediated transcriptional activation. Knockdown of SUV39H1 in patient-derived GSCs impaired their proliferation and stemness. RNA-seq analysis revealed that SUV39H1 regulates G2/M cell cycle progression, stem cell maintenance, and cell death pathways in GSCs. Integrated ATAC-seq (assay for transposase-accessible chromatin followed by sequencing) and RNA-seq analyses demonstrated that targeting SUV39H1 altered chromatin accessibility in key genes associated with these pathways. Treatment with chaetocin, a SUV39H1 inhibitor, mimicked the effects of SUV39H1 knockdown in GSCs and sensitized them to the GBM chemotherapy drug temozolomide (TMZ). In vivo studies using an intracranial patient-derived xenograft model showed that targeting SUV39H1 inhibited GSC-driven tumor formation in mice. Our findings identify SUV39H1 as a critical regulator of GSC maintenance and suggest that targeting SUV39H1 could disrupt GSCs and enhance the efficacy of existing chemotherapy, offering a promising strategy for improving GBM treatment outcomes.

2024-11-06 | GSE273012 | GEO

SUV39H1 Maintains Cancer Stem Cells in Glioblastoma [ATAC-seq]

2024-11-06 | GSE273013 | GEO

Effects of SUV39H1 depletion on gene expression in HeLa cells

Project description:HeLa cells were transiently transfected with siRNA against SUV39H1, a histone H3K9 methyltransferase. Several genes were significantly up- or down-regulated. HeLa cells were transiently transfected with siRNA against SUV39H1 or negative control siRNA. Then total RNA was extracted.

2015-08-01 | E-GEOD-59243 | biostudies-arrayexpress

Expression data from Adriamycin-treated Emu-myc; Suv39h1-/- B-cell lymphoma

Project description:Oncogene-induced senescence (OIS), a terminal cell cycle block countering (pre)neoplastic lesions, is characterised on the molecular level by trimethylated histone H3 lysine 9 (h3K9me3), a transcriptionally repressive chromatin mark linked to silencing of S-phase-promoting genes. Whether H3K9-governed chromatin remodelling influences anticancer treatment-induced senescence (TIS) and whether functional control of this mark impacts on treatment outcome is not known. We used global gene expression profiling by microarrays to gain insight into the molecular responses of Emu-myc; Suv39h1-/- B-cell lymphoma cells to senescence-inducing anticancer agent Adriamycin (ADR). Primary lymphoma cells isolated from lymph nodes of Emu-Myc; Suv39h1-/- mice were used. In this model, the c-Myc oncogene is constitutively expressed in the cells of the B-cell lineage, leading to spontaneous development of aggressive B-cell lymphomas. Adriamycin (ADR), a cytostatic drug used as a standard part of several lymphoma treatment regimens, is known to massively induce TIS in Suv39h1-proficient lymphomas, protected from apoptosis by Bcl-2 over expression (Myc;Bcl2). In order to discern the impact of Suv39h1 to TIS induction under these conditions, we analysed here transcriptional profiles of matched pairs of Emu-myc;Suv39h1-/-;Bcl2 lymphomas, untreated or treated for 5 days with ADR.

2013-07-04 | E-GEOD-44355 | biostudies-arrayexpress

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