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Male SD rats treated with high fat diet (HFD) and DNA methyltransferase (DNMT) inhibitor 5-aza-2'-deoxycytidine (5-AzaD)

ABSTRACT: Male SD rats treated with high fat diet (HFD) and DNA methyltransferase (DNMT) inhibitor 5-aza-2'-deoxycytidine (5-AzaD)

PROVIDER: PRJNA272548 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR1755930_1.fastq.gz	Fastqsanger.gz
	SRR1755930_2.fastq.gz	Fastqsanger.gz
	SRR1755940_1.fastq.gz	Fastqsanger.gz
	SRR1755940_2.fastq.gz	Fastqsanger.gz
	SRR1755960.fastq.gz	Fastqsanger.gz

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DNA methylation profile for male SD rats treated with high fat diet (HFD) and DNA methyltransferase (DNMT) inhibitor 5-aza-2′-deoxycytidine (5-AzaD) by RRBS

Project description:To investigate the effects of HFD on affecting the DNA methylation, as well as the methylation inhibitor 5-AzaD reversing such effects in the frontal cortex of male SD rats by sequencing the methylome (RRBS).

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Gene expression profile for male SD rats treated with high fat diet (HFD) and DNA methyltransferase (DNMT) inhibitor 5-aza-2′-deoxycytidine (5-AzaD) by RNA-Seq

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MCF7 cells gene expression change by inducing CpG demethylation using 5-Aza-2'-deoxycytidine (Aza)

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SUMO pulldown proteomics Namalwa 5-Aza-2' deoxycytidine treatment

Project description:Combination therapies targeting malignancies aim to increase treatment efficacy and reduce toxicity. Hypomethylating drug 5-Aza-2’-deoxycytidine (5-Aza-2’) enhances transcription of tumor suppressor genes and induces replication errors via entrapment of DNMT1. Post-translational modification by SUMO plays major roles in the DNA damage response and is required for degradation of entrapped DNMT1. Here, we combine SUMOylation inhibitor TAK981 and DNA-hypomethylating agent 5-Aza-2’ to improve treatment of MYC driven hematopoietic malignancies, since MYC overexpressing tumors are sensitive to SUMOylation inhibition. We studied the classical MYC driven malignancy Burkitt lymphoma, as well as diffuse large B-cell lymphoma (DLBCL) with and without MYC translocation. SUMO inhibition prolonged the entrapment of DNMT1 to DNA, resulting in DNA damage. An increase in DNA damage was observed in cells co-treated with TAK981 and 5-Aza-2’. Both drugs synergized to reduce cell proliferation in vitro in a B cell lymphoma cell panel, including Burkitt lymphoma and DLBCL. In vivo experiments combining TAK981 (25 mg/kg) and 5-Aza-2’ (2.5 mg/kg) showed a significant reduction in outgrowth of Burkitt lymphoma in an orthotopic xenograft model. In contrast, single dosing of TAK981 was ineffective and single dosing of 5-Aza-2’ only led to a modest outgrowth reduction. TAK981 and 5-Aza-2’ synergize to reduce B cell Lymphoma outgrowth in vitro and in vivo. SUMOylation is a key-player in the repair of DNA damage, hence upon TAK981 treatment the repair of DNA damage induced by 5-Aza-2’ treatment is impaired. Our results demonstrate the potential of tailored combination of drugs, based on insight in molecular mechanisms, to improve the efficacy of cancer therapies.

2023-03-17 | PXD038620 | Pride

Impact of 5-Aza-2`-deoxycytidine and Epigallocatechin-3-gallate for induction of human regulatory T cells

Project description:The epigenetic regulation of transcription factor genes is critical for T cell lineage specification. A specific methylation pattern within a conserved region of the lineage specifying transcription factor gene FOXP3, the Treg-specific demethylated region (TSDR), is restricted to regulatory T (Treg) cells and required for stable expression of FOXP3 and suppressive function. We analyzed the impact of hypomethylating agents 5-Aza-2`-deoxycytidine and Epigallocatechin-3-gallate (EGCG) on human CD4+CD25- T for generating Treg cell specific DNA methylation pattern within FOXP3-TSDR and inducing functional Treg cells. Gene expression, including lineage specifying transcription factors of the major T cell lineages and their leading cytokines, functional properties and global transcriptome changes were analyzed. 5-Aza-2`-deoxycytidine induced FOXP3-TSDR methylation and expression of Treg cell specific genes FOXP3 and LRRC32. Proliferation of 5-Aza-2´deoxycytidine treated cells was reduced, but they did not show suppressive function. Hypomethylation was not restricted to FOXP3-TSDR and expression of master transcription factors and leading cytokines of Th1 and Th17 cells were induced. EGCG induced global DNA hypomethylation to a lower degree than 5-Aza-2´deoxycitidine, but no relevant hypomethylation within FOXP3-TSDR or expression of Treg cell specific genes. Both DNMT inhibitors did not induce full functional human Treg cells. Although 5-Aza-2`-deoxycytidine treated cells phenotypically appeared to be Treg cells, they did not suppress proliferation of responder cells, which is an essential capability to be used in Treg cell transfer therapy.

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MCF7 cells gene expression change by inducing CpG demethylation using 5-Aza-2'-deoxycytidine (Aza)

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SUMO pulldown, U2OS, proteomics, 4 hour 20 hour 5-Aza-2' deoxycytidine treatment

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