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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

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

PROVIDER: PRJNA875444 | ENA |

REPOSITORIES: ENA

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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 [RNA-seq]

Project description: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]

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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]

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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]

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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]

Project description: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.

2025-08-18 | GSE212437 | 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 [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

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

2025-08-18 | GSE212452 | 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.

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Nrf2 transcript alterations

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Pyrimethamine and a potent analogue WCDD115 inhibit NRF2 by suppressing DHFR and one-carbon metabolism

Project description:Nuclear factor erythroid 2-related factor 2 (NFE2L2/NRF2) is a critical mediator of the cellular oxidative stress response. Aberrant activation of NRF2 is common in many lung and upper aerodigestive cancers, where it promotes tumor progression and confers resistance to chemotherapy, radiation therapy, and immune checkpoint inhibitors. As such, NRF2 therapeutic inhibitors are actively being sought. We previously reported that the antiparasitic drug Pyrimethamine (PYR) inhibits NRF2 in cells and in an NRF2-inducible genetically engineered mouse model. Here we design, synthesize, and define structure-activity relationships across a series of 25 PYR-based derivatives to reveal WCDD115 as a 22-fold more potent inhibitor of NRF2 (57nM versus 1.2mM). PYR is known to inhibit plasmodial and human dihydrofolate reductase (DHFR). We found that WCDD115 inhibits hDHFR with 31-fold greater potency than PYR (144nM versus 4.49mM). Metabolomics showed strong similarities between PYR, WCDD115 and methotrexate. Genetic, pharmacological and metabolic epistasis studies reveal that DHFR inactivation is required for NRF2 suppression by WCDD115 and PYR. Global and targeted proteomics revealed overlapping profiles for WCDD115, PYR and methotrexate, including suppression of NRF2 oxidative stress response and activation of TP53 and the DNA damage response. As such, PYR and its more potent derivative WCDD115 are effective, indirect inhibitors of NRF2 and its antioxidant functions. These data underscore the importance of one-carbon metabolism for the NRF2 signaling pathway and supports a new therapeutic strategy to suppress NRF2-driven cancer biology.

2025-10-13 | PXD059011 | Pride

Quantitative profiling of DNA 6mA at single-base resolution using NAME-seq I

Project description:DNA N6-methyladenine (6mA) is the most widespread type of DNA methylation in prokaryotes. However, the prevalence of 6mA in eukaryotes has recently been challenged due to the limitations of current 6mA detection techniques. Here, we present a chemical-based sequencing method, Nitrite-assisted Amino MEthylation sequencing (NAME-seq), for quantitative, whole-genome mapping of 6mA at single-base resolution. NAME-seq combines nitrite conversion of 6mA to nitrosylated-6mA (6mA-NO) with Klenow Fragment (3'→5' exo-) random priming to induce a 6mA-to-T transversion specifically. We apply NAME-seq to two bacterial species and show that, compared to SMRT-seq, NAME-seq results in a more specific and robust detection of 6mA. NAME-seq can also accurately map 6mA in the C. reinhardtii genome at single-base resolution. Additionally, we show that NAME-seq can be combined with conventional DIP-seq to detect 6mA in the Dam-methylated human genome with high specificity. Therefore, we further perform DIP-NAME-seq to profile 6mA in WT and TASOR KO K562 cell line and revealed that 6mA is enriched at specific motifs (HYYHAG and CACACA) and H3K9me3 regions. In summary, we demonstrate NAME-seq is a specific and sensitive sequencing method for quantitative 6mA mapping at single base resolution across different model organisms.

2025-10-09 | GSE215168 | GEO

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