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GSF1243: RNA-seq data of adipocytes treated with DNMT1 inhibitor, guadecitabine (100nM), for 3 days

ABSTRACT: GSF1243: RNA-seq data of adipocytes treated with DNMT1 inhibitor, guadecitabine (100nM), for 3 days

OTHER RELATED OMICS DATASETS IN: GSE111305

PROVIDER: PRJNA436558 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6794970.fastq.gz	Fastqsanger.gz
	SRR6794971.fastq.gz	Fastqsanger.gz
	SRR6794972.fastq.gz	Fastqsanger.gz
	SRR6794973.fastq.gz	Fastqsanger.gz

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GSF1243: RNA-seq data of adipocytes treated with DNMT1 inhibitor, guadecitabine (100nM), for 3 days

Project description:Ovarian cancer (OC) cells frequently metastasize to the omentum and adipocytes play a significant role in ovarian tumor progression. Therapeutic interventions targeting aberrant DNA methylation in ovarian tumors have shown promise in the clinic but the effects of epigenetic therapy on the tumor microenvironment are understudied. Here, we examined the effect of adipocytes on OC cell behavior in culture and impact of targeting DNA methylation in adipocytes on OC metastasis. The presence of adipocytes increased OC cell migration and invasion and proximal and direct co-culture of adipocytes .increased OC proliferation alone or after treatment with carboplatin. Treatment of adipocytes with hypomethylating agent guadecitabine decreased migration and invasion of OC cells towards adipocytes. Due to this result, we performed RNA-seq of adipocytes treated with DNMT1 inhibitor to analyze differential gene expression changes that occur in the adipocyte that may explain the above observation that hypomethylating agent treatment of adipocytes decrease migration and invasion.

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DNA methylation profile of adipocytes treated with DNMT inhibitor, guadecitabine (100nM, 3X daily).

Project description:DNA methylation profile of adipocytes treated with DNMT inhibitor, guadecitabine (100nM, 3X daily).

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DNA methylation profile of adipocytes treated with DNMT inhibitor, guadecitabine (100nM, 3X daily).

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Project description:White adipose tissue (WAT) is a key regulator of systemic energy metabolism, and impaired WAT plasticity characterized by enlargement of preexisting adipocytes associates with WAT dysfunction, obesity and metabolic complications. However, the mechanisms that retain proper adipose tissue plasticity required for metabolic fitness are unclear. Here, we comprehensively showed that adipocyte-specific DNA methylation, manifested in enhancers and CTCF sites, directs distal enhancer-mediated transcriptomic features required to conserve metabolic functions of white adipocytes. Particularly, genetic ablation of adipocyte Dnmt1, the major methylation writer, led to increased adiposity characterized by increased adipocyte hypertrophy along with reduced expansion of adipocyte precursors (APs). These effects of Dnmt1 deficiency provoked systemic hyperlipidemia and impaired energy metabolism both in lean and obese mice. Mechanistically, Dnmt1 deficiency abrogated mitochondrial bioenergetics by inhibiting mitochondrial fission and promoted aberrant lipid metabolism in adipocytes, rendering adipocyte hypertrophy and WAT dysfunction. Dnmt1-dependent DNA methylation prevented aberrant CTCF binding and, in turn, sustained the proper chromosome architecture to permit interactions between enhancer and dynamin-related protein gene Drp1 in adipocytes. Also, adipose DNMT1 expression inversely correlated with adiposity and markers of metabolic health, but positively correlated with AP-specific markers in obese human subjects. Thus, these findings support strategies utilizing Dnmt1 action on mitochondrial bioenergetics in adipocytes to combat obesity and related metabolic pathology.

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