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Epigenetic reprogramming of melanoma cells by vitamin C treatment

ABSTRACT: Epigenetic reprogramming of melanoma cells by vitamin C treatment

PROVIDER: PRJNA495630 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7995443_1.fastq.gz	Fastqsanger.gz
	SRR7995443_2.fastq.gz	Fastqsanger.gz
	SRR7995444_1.fastq.gz	Fastqsanger.gz
	SRR7995444_2.fastq.gz	Fastqsanger.gz
	SRR7995445_1.fastq.gz	Fastqsanger.gz

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Epigenetic reprogramming of melanoma cells by vitamin C treatment

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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.

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Vitamin C deficiency causes cell type-specific epigenetic reprogramming and acute tubular necrosis

Project description:The recently described roles of vitamin C as an epigenetic regulator playsa crucial role in normal physiological development and pathological conditions.However, the epigenetic regulatory role of vitamin C in renal homeostasis andpathogenesis remains largely unknown. We aim to reveal that vitamin C deficiency promoted acute tubular necrosis,and provide a potential mechanism for epigenetic therapy in preventing the progression of chronic kidney disease.

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Oct4 and jhdm1b infected MEF with or without vitamin C treatment

Project description:Investigate the effect of jhdm1b on Oct4 mediated reprogramming Investigate the effect of vitamin C on the function of jhdm1b oct4 and jhdm1b infected MEF with or without vitamin C treatment

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Vitamin C deficiency causes cell type-specific epigenetic reprogramming and acute tubular necrosis

Project description:Vitamin C deficiency causes cell type-specific epigenetic reprogramming and acute tubular necrosis

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Epigenetic reprogramming shapes the cellular landscape of schwannoma

Project description:Cell state evolution underlies tumor development and response to therapy1, but mechanisms specifying cancer cell states and intratumor heterogeneity are incompletely understood. Schwannomas are the most common tumors of the peripheral nervous system and are treated with surgery and ionizing radiation2–5. Schwannomas can oscillate in size for many years after radiotherapy6,7, suggesting treatment may reprogram schwannoma cells or the tumor microenvironment. Here we show epigenetic reprogramming shapes the cellular landscape of schwannomas. We find schwannomas are comprised of 2 molecular groups distinguished by reactivation of neural crest development pathways or misactivation of nerve injury mechanisms that specify cancer cell states and the architecture of the tumor immune microenvironment. Schwannoma molecular groups can arise independently, but ionizing radiation is sufficient for epigenetic reprogramming of neural crest to immune-enriched schwannoma by remodeling chromatin accessibility, gene expression, and metabolism to drive schwannoma cell state evolution and immune cell infiltration. To define functional genomic mechanisms underlying epigenetic reprograming of schwannomas, we develop a technique for simultaneous interrogation of chromatin accessibility and gene expression coupled with genetic and therapeutic perturbations in single-nuclei. Our results elucidate a framework for understanding epigenetic drivers of cancer evolution and establish a paradigm of epigenetic reprograming of cancer in response to radiotherapy.

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Project description:We found a small molecule-DKG, relative to Vitamin C, could replace the function of Viamin C during reprogramming. After comparing transcriptome profiling (RNA-seq) of this molecule to vitamin C, it could provide a framework for more mechanism.

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