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ABSTRACT: TET1 regulates hypoxia-induced epithelial-mesenchymal transition through DNA demethylation

PROVIDER: PRJNA257214 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR1533840.fastq.gz	Fastqsanger.gz
	SRR1533841.fastq.gz	Fastqsanger.gz
	SRR1533842.fastq.gz	Fastqsanger.gz
	SRR1533843.fastq.gz	Fastqsanger.gz
	SRR1533836.fastq.gz	Fastqsanger.gz

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Project description:TET1 regulates hypoxia-induced epithelial-mesenchymal transition through DNA demethylation (hMeDIP-Seq)

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Project description:TET1 regulates hypoxia-induced epithelial-mesenchymal transition through DNA demethylation (RNA-Seq)

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H3K36me3-coupled DNA Demethylation by DNMT3A Is Essential for Hypoxia-Induced EMT of Cancer Cells [ChIP-Seq]

Project description:The epithelial-to-mesenchymal transition (EMT) and metastasis of the cancer cells are closely associated with epigenetic changes of chromatin and reprogramming of transcriptomes. The DNA methyltransferases DNMT3A and DNMT3B possess DNA demethylation/dehydroxymethylation activities. Here, we show, by a range of molecular/cellular approaches, that active DNA demethylation activity of DNMT3A is required for hypoxia-induced EMT of the primary colon carcinoma SW480 cells, its genome-wide DNA demethylation, and promoter DNA demethylation/transcriptional activation of the EMT genes TWIST1 and SNAIL1. DNMT3A also positively regulates hypoxia-induced TWIST1 activation in other types of cancer cells. Mechanistic analysis supports a regulatory model, in which hypoxia-induced H3K36me3 mark recruits DNMT3A to demethylate CpG in the hypoxia-responsive element (HRE), thereby facilitating HIF-1α binding and TWIST1 activation. This study demonstrates for the first time an in vivo functional role of the active DNA demethylation activity of DNMT3A and its potential as a novel therapeutic target of anti-cancer development.

2025-08-13 | GSE252166 | GEO

H3K36me3-coupled DNA Demethylation by DNMT3A Is Essential for Hypoxia-Induced EMT of Cancer Cells [Bisulfite Sequencing]

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Hypoxia-induced CTCF mediates alternative splicing via coupling chromatin looping and RNA Pol II pause to promote EMT in breast cancer

Project description:Cancer cells experiencing hypoxic stress employ epithelial-mesenchymal transition (EMT) to undergo metastasis through rewiring of the chromatin landscape, epigenetics and importantly alternative splicing. However, how hypoxia influences expression and genome-wide redistribution of CTCF is still not known. Here, we performed CTCF-ChIP-seq and CUT&RUN assay to analyze differential occupancy of CTCF in normoxic and hypoxic breast cancer cell line. We discovered that hypoxia-induced gain of CTCF occupancy across the genome regulates EMT in hypoxic cells. Specifically, we did 4C-seq experiments on COL5A1 (EMT associated gene) gene loci and showed that CTCF-mediated promoter-exon upstream looping regulates epigenetic mark mainly DNA demethylation at distal alternatively spliced exon 64 and regulates CTCF-mediated RNA Pol II pausing at COL5A1exon64A that decides the outcome of splicing to favor EMT under hypoxia. Overall, we uncover that hypoxia-induced differential CTCF occupancy across the genome is associated with gene expression and alternative splicing events related to cancer progression, similarly to the proposed model.

2024-12-31 | GSE216843 | GEO

TET1 regulates hypoxia-induced epithelial-mesenchymal transition through DNA demethylation (hMeDIP-Seq)

Project description:In order to explore the status of DNA methylation in hypoxia response, we show that TET1, a DNA dioxygenase converting 5-methylcytosine (5mC) into 5-hydroxymethylcytosine (5hmC), regulates hypoxia-responsive gene expression. Hypoxia/HIF-2Î± regulates the expression of TET1. Knockdown of TET1 mitigated hypoxia-induced EMT. RNA sequencing and 5hmC sequencing identified the set of TET1-regulated genes. Four samples (Four samples, Hypoxia (scrambled control), Hypoxia (TET1-si), Normoxia (scrambled control) and Normoxia (TET1-si), are performed by RNA-Seq and hMeDIP-Seq

2014-08-01 | E-GEOD-59989 | biostudies-arrayexpress

TET1 regulates hypoxia-induced epithelial-mesenchymal transition through DNA demethylation (RNA-Seq)

2014-08-01 | E-GEOD-59987 | biostudies-arrayexpress

Tet1 as a Negative Regulator of Somatic Cell Reprogramming

Project description:Tet1 is a hydroxylase known for its role in the conversion of 5-methylcytosines (5mC) to 5-hydroxymethylcytosines (5hmC) involved in the possible active demethylation process and gene expression regulation1-5.M-BM- As somatic cell reprogramming involves the re-activation of pluripotency genes and the silencing of somatic ones6, it remains unclear whether Tet1 plays a positive or negative role in the reprogramming process. Here we show that Tet1 deficiency enhances reprogramming and its overexpression impairs reprogramming. Mechanistically, we demonstrated that Tet1 represses the early obligatory process of mesenchymal to epithelial transition (MET) during reprogramming7,8. Thus, our findings not only define a negative role for Tet1 in somatic cell reprogramming, but also suggest that the Tet enzymes regulate cell fate through distinctive mechanisms. Examination of genome DNA hmC modifications in 2 conditions: individually overexpressed Tet1CD or Tet2CD during MEF reprogramming; Examination of mRNA levels in five different conditions: individually overexpressed DR or Tet1CD or Tet1CDmut or Tet2CD or Tet2CDmut, during MEF reprogrammig.

2013-03-08 | E-GEOD-44935 | biostudies-arrayexpress