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Gene Expression Profiling of human and mouse melanoma cell lines after shRNA-mediated knockdown of JMJD2C or LSD1

ABSTRACT: Gene Expression Profiling of human and mouse melanoma cell lines after shRNA-mediated knockdown of JMJD2C or LSD1

PROVIDER: PRJNA415006 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6188752.fastq.gz	Fastqsanger.gz
	SRR6188743.fastq.gz	Fastqsanger.gz
	SRR6188753.fastq.gz	Fastqsanger.gz
	SRR6188744.fastq.gz	Fastqsanger.gz
	SRR6188754.fastq.gz	Fastqsanger.gz

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Gene Expression Profiling of melanoma cell lines after shRNA-mediated knockdown of JMJD2C or LSD1

Project description:We hypothesize that knockdown of the H3K9 demethylases JMJD2C or LSD1 results in decreased proliferation and tumorigenic potential

2017-12-04 | GSE105137 | GEO

Gene Expression Profiling of melanoma cell lines after shRNA-mediated knockdown of JMJD2C or LSD1

Project description:Gene Expression Profiling of melanoma cell lines after shRNA-mediated knockdown of JMJD2C or LSD1

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Gene Expression Profiling of one melanoma cell line after shRNA-mediated knockdown of JMJD2C or LSD1

Project description:We hypothesize that knockdown of the H3K9 demethylases JMJD2C or LSD1 results in decreased proliferation and tumorigenic potential

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Gene Expression Profiling of one melanoma cell line after shRNA-mediated knockdown of JMJD2C or LSD1

Project description:Gene Expression Profiling of one melanoma cell line after shRNA-mediated knockdown of JMJD2C or LSD1

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Lactylation of LSD1 is an acquired epigenetic vulnerability of BRAFi/MEKi-resistant melanoma

Project description:BRAFV600E mutant melanomas treated with BRAF inhibitor (Dabrafenib) and MEK inhibitor (Trametinib) almost invariably develop drug resistance (DTR). Restored glycolysis has been frequently found in clinical targeted therapy-resistant melanoma biopsies. LDH, catalyzing the last step of glycolysis, is negatively correlated with clinical outcome of melanoma patients receiving BRAFi target therapy. How resumed glycolysis controls the emergence of acquired resistance, especially via intrinsic mechanisms that circumvent the BRAF/MEK module, remains unknown. Here, we identify lactylation of LSD1, induced by re-accumulated lactate in DTR melanoma cells, selectively drives survival via epigenetic reprogramming. Mechanistically, lactylation of LSD1 promotes its interaction with FosL1, thereby preventing its ubiquitination and degradation by E3 ligase tripartite-motif-containing protein 21 (TRIM21). In DTR melanoma cells, chromatin binding capacity of FosL1 was significantly strengthened due to reduced acetylation, which in turn increases selective chromatin enrichment of LSD1. We further demonstrate that lactylated LSD1 co-orchestrates gene transcription with FosL1 to repress ferroptosis in DTR cells via interfering with transferrin receptor protein 1 (TFRC)-mediated iron uptake. LSD1 inhibitor (LSD1i) activates ferroptosis, resulting in drastic DTR melanoma regression in mice. Importantly, LSD1i-induced immunogenic ferroptosis synergizes with immune checkpoint blockade (ICB) in vivo. Together, our results highlight a crucial role of metabolic rewiring-induced epigenetic reprogramming as a bypass resistance mechanism in DTR melanoma, which provides a therapeutically actionable strategy to overcome acquired resistance to targeted therapy.

2024-03-04 | PXD050308 |

Gene Expression Profiling of human and mouse melanoma cell lines after shRNA-mediated knockdown of JMJD2C or LSD1

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

2017-12-04 | GSE105166 | GEO

Jmjd1a / Jmjd2c RNAi expression profile

Project description:Global gene expression effects of silencing Jmjd1a and Jmjd2c genes We used microarrays to detail the global programme of gene expression after silencing Jmjd1a gene and Jmjd2c gene separately Keywords: dose response

2007-09-29 | GSE8937 | GEO

Lactylation of LSD1 is an acquired epigenetic vulnerability of BRAFi/MEKi-resistant melanoma [ChIP-seq]

Project description:BRAFV600E mutant melanomas treated with BRAF inhibitor (Dabrafenib) and MEK inhibitor (Trametinib) almost invariably develop drug resistance (DTR). Restored glycolysis, frequently found in clinical targeted therapy-resistant melanoma biopsies, has been shown to elicit drug resistance. How resumed glycolysis controls the emergence of acquired resistance, especially via intrinsic mechanisms that circumvent the BRAF/MEK module, remains unknown. Here, we identify lactylation of LSD1, induced by re-accumulated lactate in DTR melanoma cells, selectively drives survival via epigenetic reprogramming. Mechanistically, lactylation of LSD1 promotes its interaction with FosL1, thereby preventing its ubiquitination and degradation by E3 ligase tripartite-motif-containing protein 21 (TRIM21). In DTR melanoma cells, chromatin binding capacity of FosL1 was significantly strengthened due to reduced acetylation, which in turn increases selective chromatin enrichment of LSD1. We further demonstrate that lactylated LSD1 co-orchestrates gene transcription with FosL1 to repress ferroptosis in DTR cells via interfering with transferrin receptor protein 1 (TFRC)-mediated iron uptake. LSD1 inhibitor (LSD1i) activates ferroptosis, resulting in drastic DTR melanoma regression in mice. Importantly, LSD1i-induced immunogenic ferroptosis synergizes with immune checkpoint blockade (ICB) in vivo. Together, our results highlight a crucial role of metabolic rewiring-induced epigenetic reprogramming as a bypass resistance mechanism in DTR melanoma, which provides a therapeutically actionable strategy to overcome acquired resistance to targeted therapy.

2025-02-13 | GSE256123 | GEO

Lactylation of LSD1 is an acquired epigenetic vulnerability of BRAFi/MEKi-resistant melanoma [RNA-seq]

Project description:BRAFV600E mutant melanomas treated with BRAF inhibitor (Dabrafenib) and MEK inhibitor (Trametinib) almost invariably develop drug resistance (DTR). Restored glycolysis, frequently found in clinical targeted therapy-resistant melanoma biopsies, has been shown to elicit drug resistance. How resumed glycolysis controls the emergence of acquired resistance, especially via intrinsic mechanisms that circumvent the BRAF/MEK module, remains unknown. Here, we identify lactylation of LSD1, induced by re-accumulated lactate in DTR melanoma cells, selectively drives survival via epigenetic reprogramming. Mechanistically, lactylation of LSD1 promotes its interaction with FosL1, thereby preventing its ubiquitination and degradation by E3 ligase tripartite-motif-containing protein 21 (TRIM21). In DTR melanoma cells, chromatin binding capacity of FosL1 was significantly strengthened due to reduced acetylation, which in turn increases selective chromatin enrichment of LSD1. We further demonstrate that lactylated LSD1 co-orchestrates gene transcription with FosL1 to repress ferroptosis in DTR cells via interfering with transferrin receptor protein 1 (TFRC)-mediated iron uptake. LSD1 inhibitor (LSD1i) activates ferroptosis, resulting in drastic DTR melanoma regression in mice. Importantly, LSD1i-induced immunogenic ferroptosis synergizes with immune checkpoint blockade (ICB) in vivo. Together, our results highlight a crucial role of metabolic rewiring-induced epigenetic reprogramming as a bypass resistance mechanism in DTR melanoma, which provides a therapeutically actionable strategy to overcome acquired resistance to targeted therapy.

2025-02-13 | GSE256122 | GEO

Combinatorial role of Jmjd2b and Jmjd2c in mESCs identity

Project description:Genome-wide occupancy of biotinylated Jmjd2b, Jmjd2c from mESCs, as well as occupancy of selected factors and histone marks from wild-type mESCs, Anti-GFP KD, Jmj2b KD and Jmjd2c KD mESCs genome To identify genome-wide binding target sites of Jmjd2b and Jmjd2c in the mESCs genome, and genome-wide binding sites for selected factors and histone marks from Anti-GFP KD, Jmjd2b KD and Jmjd2c KD mESCs

2013-12-01 | E-GEOD-43229 | biostudies-arrayexpress

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