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EZH2 reads DNA 6mA to regulate survival and drug resistance of human head and neck squamous carcinoma by suppressing RIOX2-CDKN1A-NRF2 signaling axis [MeDIP-ChIP-seq-shRNA]

ABSTRACT: To determine whether 6mA has a role in guiding EZH2 recruitment, we focused on ALKBH1, the well-defined DNA 6mA demethylase in mammals, and knocked down ALKBH1 expression in HNSCC cells using shRNAs. We performed MeDIP-seq and ChIP-seq using these cells, and found that ALKBH1 deletion led to an obvious gain of 6mA peaks, which accompanied with enrichment of EZH2 and H3K27me3.

ORGANISM(S): Homo sapiens

PROVIDER: GSE212437 | GEO | 2025/08/18

REPOSITORIES: GEO

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EZH2 reads DNA 6mA to regulate survival and drug resistance of human head and neck squamous carcinoma by suppressing RIOX2-CDKN1A-NRF2 signaling axis [ChIP-MeDIP-seq]

Project description:we attempted to comprehensively assess whether EZH2 recognizes 6mA modification at the global level. We first performed chromatin immunoprecipitation following sequencing (ChIP-seq) in human HNSCCs using antibody that recognize EZH2 to determine its genome-wide occupancies.We further investigated 6mA profiling using methylated DNA immunoprecipitation following sequencing (MeDIP-seq).

2025-08-18 | GSE212400 | GEO

EZH2 reads DNA 6mA to regulate survival and drug resistance of human head and neck squamous carcinoma by suppressing RIOX2-CDKN1A-NRF2 signaling axis [RNA-seq]

Project description:We performed short hairpin RNA (shRNA)-mediated knockdown (KD) experiments to abrogate ALKBH1 expression. To comprehensively understand the underlying mechanism of ALKBH1 in HNSCC, we performed RNA-seq assay and profiled gene expression alteration of HNSCC cells upon ALKBH1 knockdown.

2025-08-18 | GSE212451 | GEO

EZH2 reads DNA 6mA to regulate survival and drug resistance of human head and neck squamous carcinoma by suppressing RIOX2-CDKN1A-NRF2 signaling axis

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

2025-08-18 | GSE212452 | GEO

Reduction N6AMT1-mediated 6mA DNA modification promotes tumor progression [MeDIP-seq]

Project description:Reduction N6AMT1-mediated 6mA DNA modification promotes tumor progression [MeDIP-seq]

| PRJNA701301 | ENA

Reduction N6AMT1-mediated 6mA DNA modification promotes tumor progression [MeDIP-seq]

Project description:Background: DNA N6-methyladenosine (6mA) as a novel epigenetic signaling modification in humans and has been implicated in progression and tumorigenesis of several cancers. However, the function and mechanisms of 6mA in breast cancer (BC), the most common cancer among women, are unclear. Methods: The clinical role of 6mA was investigated by immunohistochemical (IHC) staining and Kaplan-Meier analysis of BC and their normal tissues. 6mA immunoprecipitation (IP) sequencing, mRNA sequencing and bioinformatics analysis were used to screen and validate the direct targets of 6mA. Results: Decreases in N6AMT1 correlated with the extent of 6mA in BC tissues and predicted a worse overall survival of BC patients. Knockdown N6AMT1 markedly reduced 6mA in DNA and promoted the proliferation and migration of BC in vivo and in vitro, whereas overexpression of N6AMT1 had the opposite effect, indicating N6AMT1 is a functional methyltransferase for DNA 6mA and relates with gene transcription. Critical negative regulators of the cell cycle, such as RB1, P21, REST and TP53 were identified as targets of N6AMT1 in BC. Conclusion: These results suggest N6AMT1 enhances DNA 6mA levels to repress tumor progression via transcriptional regulation of cell cycle inhibitors.

2022-03-31 | GSE166580 | GEO

Fox Family Protein Jumu Reads 6mA-DNA Codes and Contributes to Zygotic Gene Activation

Project description:N6-methyladenine (6mA) DNA modification in eukaryotic genomes has emerged as a potential epigenetic mark. However, little is known about how 6mA epigenetic codes are read and interpreted in higher eukaryotes. Here we investigate 6mA genome-wide distributions in multiple higher eukaryotes. Using Drosophila as a pioneer system, we show that 6mA exhibits defined patterns and preferentially marks zygotic genes in early embryos. Moreover, we identify that the Fox-family protein, Jumu, is a "6mA-DNA reader" and functions in concert with DMAD to contribute to zygotic gene activation. Further methylome analysis reveals that 6mA modification has common features in genomic DNA from mouse, rat and monkey, and that "forkhead-domain-binding motifs" are enriched in 6mA-marked DNA of these genomes, in a way similar to Drosophila. Collectively, our findings identify the 6mA DNA reader protein and suggest a conserved 6mA-based mechanism in higher eukaryotes.

2023-01-14 | GSE90720 | GEO

Genome wide 6mA modification change upon mitochondial stress in C.elegans

Project description:We discovered 364 peaks enrichment change in wild-type C.elegans genome by 6mA MeDIP-seq, which indicated those genes response to mitochondrial stress and may function in mitochondrial stress response.

2018-09-27 | GSE118268 | GEO

ALKBH1 deficiency leads to loss of homeostasis in human diploid somatic cells

Project description:DNA N6-methyladenosine (6mA) in eukaryotic genomes has recently been observed in diverse species. 6mA has been reported to associate with multiple physiological processes including embryonic development and tumorigenesis, and ALKBH1 is a primary 6mA demethylase in mouse and human cells. To research the roles of 6mA and its putative regulators such as putative ALKBH1 in the homeostatic maintenance of human stem cells and their differentiated derivatives, We generated ALKBH1-deficient human embryonic stem cells (hESCs) via CRISPR/Cas9-mediated non-homologous end joining (NHEJ). We next differentiated ALKBH1+/+ and ALKBH1-/- hESCs into human mesenchymal stem cells (hMSCs) and vascular smooth muscle cells (hVSMCs). Early-onset growth arrest of ALKBH1-/- hMSCs was observed, and increased apoptosis and enhanced migration ability were observed in ALKBH1-/- hVSMCs. However, liquid chromatography coupled with tandem mass spectrometry (LC-MS/MS) analysis revealed no change in 6mA levels between ALKBH1+/+ and ALKBH1-/- hESCs, between ALKBH1+/+ and ALKBH1-/- hMSCs, and between ALKBH1+/+ and ALKBH1-/- hVSMCs, respectively. These data demonstrate that depletion of ALKBH1 exerts minimal impact on 6mA levels in hESCs and their differentiated derivatives and that ALKBH1 regulates the homeostasis of hMSCs and hVSMCs possibly in a DNA 6mA-independent manner.

2020-05-22 | GSE150936 | GEO

Genome-wide maps of ALKBH1 binding sites in mouse primary hepatocytes

Project description:AlkB homolog 1 (ALKBH1) has been reported to act as a DNA 6mA demethylase to remove 6mA modification in eukaryotic genomes. Our previous data showed downregulated ALKBH1 in mouse and human fatty liver and increased DNA 6mA levels in mouse fatty liver. We developed liver-specific ALKBH1 knockout (AKO) mice to directly study the role of ALKBH1 mediated DNA 6mA modification during the development of hepatic steatosis. Deletion of liver ALKBH1 promoted hepatic steatosis and insulin resistance. Overexpression of ALKBH1 resulted in opposite phenotypes. To investigate the mechanism of ALKBH1 in regulating target gene expression. We performed ChIP-seq for identifying ALKBH1 binding sites on mouse hepatocytes genomes and validated its demethylase activity for DNA 6mA modification on the target genes via ChIP-qPCR assays.

2022-10-26 | GSE197185 | GEO

Regulation of Liver metabolism by ALKBH1

Project description:AlkB homolog 1 (ALKBH1) has been reported to act as a DNA 6mA demethylase to remove 6mA modificatione in ukaryotic genomes. Our previous data showed downregalted ALKBH1 in mouse and human fatty liver and increased DNA 6mA levels in mouse fatty liver. We hypothesize that ALKBH1 may be involved in hepatic lipid metabolism. To test this hypothesis, we generated liver-specific ALKBH1 knockout (Alkbh1 f/f, Albumine-cre; AKO) mice and used high-throughput RNA sequence and other assays to directly study the role of ALKBH1 during the development of hepatic steatosis.

2022-10-26 | GSE193497 | GEO

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