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Maintenance of histone crotonylation by YEATS2 and GCDH drives EMT in head and neck cancer [ChIP-seq]

ABSTRACT: Maintenance of histone crotonylation by YEATS2 and GCDH drives EMT in head and neck cancer [ChIP-seq]

PROVIDER: PRJNA1154002 | ENA |

REPOSITORIES: ENA

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Maintenance of histone crotonylation by YEATS2 and GCDH drives EMT in head and neck cancer [RNA-seq]

Project description:Regulation of gene expression is an integral cellular process, fine-tuned by epigenetic marks like histone modifications. Perturbations in the activity or abundance of epigenetic factors can lead, or contribute to tumorigenesis in healthy cells. Remarkably, the addition of epigenetic marks is dependent on the metabolites produced during several essential cellular pathways. Here, we have explored the interplay between a highly expressed epigenetic factor YEATS2, and a metabolic enzyme GCDH in regulating epithelial to mesenchymal transition in head and neck cancer. We report the results of RNA-seq in YEATS2-silenced BICR10 cells to investigate the effect of YEATS2 in influencing gene expression globally. We have also performed ChIP-seq using YEATS2 antibody in BICR10 cells to obtain the globally occupied sites of YEATS2. Lastly, we report the changes in crotonylation at histone 3 lysine 27 (H3K27Cr) upon YEATS2 downregulation in BICR10 by performing ChIP-seq in shControl vs. shYEATS2 cells.

2025-07-15 | GSE275977 | GEO

Maintenance of histone crotonylation by YEATS2 and GCDH drives EMT in head and neck cancer [ChIP-seq]

2025-07-15 | GSE275975 | GEO

Maintenance of histone crotonylation by YEATS2 and GCDH drives EMT in head and neck cancer [RNA-seq]

Project description:Maintenance of histone crotonylation by YEATS2 and GCDH drives EMT in head and neck cancer [RNA-seq]

| PRJNA1154005 | ENA

miRNA profiles in head and neck natural epithelial - mesenchymal phenotype cell line pair, and in TGF-β induced EMT models

Project description:Sixth generation Exiqon® locked nucleic acid miRCURY™ LNA microarrays were used to search and validate some unidentified miRNAs that regulate EMT in head and neck cancer carcinoma.

2012-06-05 | GSE38459 | GEO

YEATS2 is a selective histone crotonylation reader.

Project description: Not available

| S-EPMC4856769 | biostudies-literature

miRNA profiles in head and neck natural epithelial - mesenchymal phenotype cell line pair, and in TGF-M-NM-2 induced EMT models

Project description:Sixth generation ExiqonM-BM-. locked nucleic acid miRCURYM-bM-^DM-" LNA microarrays were used to search and validate some unidentified miRNAs that regulate EMT in head and neck cancer carcinoma. MiRNA array screening was performed to identify the differential expression of miRNAs involved in EMT in natural epithelial - mesenchymal phenotype cell line pairM-oM-<M-^HHN-4, HN-12) and in TGF-M-NM-2 induced EMT models (HN-4 TGF-M-NM-2,HN-4). HN-4 parental cell was served as the control.One M-BM-5g total RNA from sample and control was labeled with Hy5M-bM-^DM-" and Hy3M-bM-^DM-" fluorescent label, respectively, using the miRCURYM-bM-^DM-" LNA Array power labeling kit (Exiqon, Denmark) following the procedure described by the manufacturer.

2012-06-04 | E-GEOD-38459 | biostudies-arrayexpress

Histone crotonylation

Project description:Histone crotonylation

| PRJNA535529 | ENA

YEATS2 O-GlcNAcylation Promotes Chromatin Association of the ATAC complex and Lung Cancer Tumorigenesis

Project description:The intracellular O-linked N-acetylglucosamine (O-GlcNAc) modification is known to be enriched in the nucleus and in particular on chromatin, but many of its chromatin targets remain to be identified. Herein we demonstrate the O-GlcNAcylation of YEATS Domain Containing 2 (YEATS2), a subunit of the chromatin Ada-two-A-containing (ATAC) complex and a reader of histone H3K27ac. We show that YEATS2 interacts with the O-GlcNAc transferase (OGT) and further pinpoint its major O-GlcNAcylation site to be Thr604 using electron transfer dissociation mass spectrometry. O-GlcNAcylation promotes the chromatin association of YEATS2, and the affinity between YEATS2 and other ATAC components on chromatin, such as ZZZ3, GCN5 and PCAF. Downstream, YEATS2-T604A attenuated the ATAC-dependent histone H3K9ac levels and inactivated the expression of essential ribosomal genes as shown in chromatin immunoprecipitation assays. Further, xenograft experiments show that YEATS2 O-GlcNAcylation promotes lung cancer tumorigenesis. Our work reveals the critical role of YEATS2 O-GlcNAcylation in stabilizing the ATAC complex on chromatin and expands the chromatin substrates of OGT.

2025-07-28 | PXD060970 | Pride

Dopaminergic neurons are vulnerable to dysregulation of YEATS2-dependent calcium homeostasis

Project description:YEATS2, a chromatin-associated factor, is essential for maintaining dopaminergic (DA) synaptic integrity, but the underlying mechanism remains unclear. Using Drosophila, we show that neuronal depletion of YEATS2 alters brain transcriptomes, downregulating metabolic genes and upregulating G protein–coupled receptors (GPCRs). This correlates with elevated intracellular calcium levels, leading to neurobehavioral deficits and selective DA neuron loss. Crucially, genetic or pharmacological inhibition of the store-operated calcium entry channel Orai restores calcium balance and rescues DA neuron survival. These findings reveal a YEATS2-dependent epigenetic–calcium axis critical for dopaminergic neuron vulnerability.

2026-04-11 | GSE307078 | GEO

Salinomycin induces cell death and differentiation in head and neck squamous cell carcinoma stem cells despite activation of EMT and Akt

Project description:Cancer stem cells are believed to play a crucial role in cancer recurrence due to their resistance to conventional chemotherapy and capacity for self-renewal. Recent studies have reported that salinomycin, a livestock antibiotic, selectively targets breast cancer stem cells 100-fold more effectively than paclitaxel. In our study we sought to determine the effects of salinomycin on head and neck squamous cell carcinoma (HNSCC) stem cells. We show that salinomycin is able to decrease cell viability and induce apoptosis. In combination with the chemotherapeutic agents cisplatin and paclitaxel, salinomycin synergistically killed HNSCC cancer stem cells more effectively than either drug alone. Furthermore, we observed that salinomycin decreases stem cell properties as shown by a significant reduction in sphere formation and a decrease of both CD44 and BMI-1. Contrary to expectations, salinomycin caused an induction of EMT as shown by an increase in Snail and Vimentin, and a decrease in E-cadherin expression. Even though EMT was induced, salinomycin caused a decrease in invasion through a membrane. In search of a possible mechanism, the effects on the Akt pathway were explored. Interestingly, salinomycin also induced phosphorylation of Akt. Activation of EMT and Akt are both tightly associated with an increase in stemness, which brings to question the relationship between CSCs and these two fundamental pathways. Taken together, our findings indicate that salinomycin shows promise as a novel treatment for HNSCC despite an activation of EMT and Akt. MicroRNA obtained from JLO-1 cells treated for 48 hours in varying doses of salinomycin. Changes in microRNA expression are analyzed by normalizing expression values with the control sample.

2013-12-31 | E-GEOD-33196 | biostudies-arrayexpress

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