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Genome-wide analysis of gene expression after knockdown of KDM5B in melanoma cells.

ABSTRACT: Genome-wide analysis of gene expression after knockdown of KDM5B in melanoma cells.

PROVIDER: PRJNA565364 | ENA |

REPOSITORIES: ENA

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Genome-wide analysis of gene expression after knockdown of KDM5B in melanoma cells.

Project description:Analysis of the effects of KDM5B in melanoma cells at gene expression level. Knockdown of KDM5B provides important information about potential target genes of KDM5B.

2022-03-14 | GSE137393 | GEO

Genome-wide analysis of gene expression after knockdown of KDM5B in melanoma cells.

Project description:Genome-wide analysis of gene expression after knockdown of KDM5B in melanoma cells.

| PRJNA565364 | ENA

Ablation of Histone Demethylase KDM5B in Melanoma Augments Anti-Tumor Immunity through Upregulation of Retroelements [RNA-Seq YUMMER1.7-Kdm5b KO]

Project description:Purpose: Advanced melanoma patients have poor prognosis. Although immune checkpoint blockade has revolutionized treatment for melanoma patients, majority of patients do not respond. The goal of this research is to evaluate whether epigenetic therapy targeting KDM5B could overcome resistance to immunotherapy. Methods:RNA-Seq analysis of KDM5B KO mouse melanoma cell lines compared to control cells to evaluate whether KDM5B depletion induces activation of retroelements, which subsequently activates type I interferon responses. Mouse studies were conducted to evaluate whether anti-tumor immunity induced by KDM5B loss could overcome immunotherapy resistance. Results: We identified that KDM5B depletion derepress retroelement expression, which subsequently activates type I interferon response and enhances anti-tumor immunity. Loss of KDM5B could overcome resistance to anti-PD-1 immunotherapy. Conclusions: Our work characterized ablation of histone demethylase KDM5B in melanoma augments anti-tumor immunity through Upregulation of retroelements.

2021-07-25 | GSE161064 | GEO

Ablation of Histone Demethylase KDM5B in Melanoma Augments Anti-Tumor Immunity through Upregulation of Retroelements [RNA-Seq 1445-Kdm5b KO]

2021-07-25 | GSE161063 | GEO

Ablation of Histone Demethylase KDM5B in Melanoma Augments Anti-Tumor Immunity through Upregulation of Retroelements [ChIP-Seq]

2021-07-25 | GSE161062 | GEO

Ablation of Histone Demethylase KDM5B in Melanoma Augments Anti-Tumor Immunity through Upregulation of Retroelements [ChIP-seq]

2021-07-25 | GSE175542 | GEO

Ablation of Histone Demethylase KDM5B in Melanoma Augments Anti-Tumor Immunity through Upregulation of Retroelements [ATAC-seq]

2021-07-25 | GSE175574 | GEO

Genome-wide analysis of INO80 knockdown

Project description:Genome-wide analysis of INO80 knockdown

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Genome wide analysis of acral melanoma

Project description:This SuperSeries is composed of the following subset Series: GSE28909: Genome wide analysis of acral melanoma (Illumina) GSE28910: Genome wide analysis of acral melanoma (Affymetrix) Refer to individual Series

2011-12-13 | E-GEOD-28913 | biostudies-arrayexpress

Genome-wide maps of transcriptomic and epigenomic state in melanoma cell lines

Project description:A mechanistic relationship between tumor epigenetic plasticity and nongenetic adaptive resistance to therapy is described, with MAPK inhibition of BRAF-mutant melanoma cells providing the model system. Upon inhibition, these largely melanocytic cells undergo reversible cell-state changes, ultimately yielding a drug-resistant mesenchymal-like phenotype. Epigenomic and transcriptomic kinetic studies, coupled with information theory and dynamic system modeling, revealed that, after just 3-days of treatment, RelA drives chromatin remodeling to establish an epigenetic program encoding long-term phenotype changes. Specifically, RelA transcriptionally inhibits SOX10 and NFKBIE through recruiting KDM5B and HDAC1 to down-regulate histone marks H3K4me3 and H3K27ac at their promoter regions. Suppression of SOX10 mediates melanoma regression towards drug-refractory phenotypes. These findings were confirmed in melanoma patients under MAPK inhibitor treatment, providing mechanistic insights into resistance-leading epigenetic reprogramming triggered following drug exposure.

2019-09-23 | GSE134459 | GEO

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