ArticleOncogene2021
H2A.Z overexpression suppresses senescence and chemosensitivity in pancreatic ductal adenocarcinoma.
Article in Oncogene, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 42 citations in OpenAlex.
- E2F3a transcription factor mediates behavioral, cellular, and DNA-protein regulation of cocaine reward in the nucleus accumbens.Molecular psychiatry · 2026Article
- Histone Variant H2A.Z2 Hyper-Transcription Induced by E2F1 Accelerates Lung Adenocarcinoma Progression via the JAK-STAT Signaling Pathway.Thoracic cancer · 2026Article
- mChIP-seq for Multiplex and Multifactorial Epigenomic Profiling Uncovers Cancer-specific Histone Features in Cellular and Circulating Nucleosomes.bioRxiv : the preprint server for biology · 2026Article
- Histone variant H2A.Z mutant suppresses the senescence-associated secretory phenotype.bioRxiv : the preprint server for biology · 2026Article
- The role of epigenetic modifications in hematological cancers.Frontiers in oncology · 2026Review
- MicroRNAs Let-7b-5p and miR-24-3p as Potential Therapeutic Agents Targeting Pancreatic Cancer Stem Cells.International journal of molecular sciences · 2025Article
- BPTF Target Engagement by Acetylated H2A.Z Photoaffinity Probes.Biochemistry · 2025Article
- Histone variant H2A.Z cooperates with EBNA1 to maintain Epstein-Barr virus latent epigenome.mBio · 2025Article
- The "Ins and Outs and What-Abouts" of H2A.Z: A tribute to C. David Allis.The Journal of biological chemistry · 2025Article
- Characterizing the regulatory effects of H2A.Z and SWR1-C on gene expression during hydroxyurea exposure in Saccharomyces cerevisiae.PLoS genetics · 2025Article
- Mathematical strategies for predicting resistant subpopulations from scRNAseq data of a PANC-1 3D tissue model: Insight into gemcitabine resistance and TGFB1-induced invasion and EMT.Computational and structural biotechnology journal · 2025Article
- Single-cell transcriptomics identifies anFrontiers in molecular biosciences · 2025Article
- Navigating glioblastoma complexity: the interplay of neurotransmitters and chromatin.Molecular biology reports · 2024Review
- Roles of Histone H2A Variants in Cancer Development, Prognosis, and Treatment.International journal of molecular sciences · 2024Review
- H2A.Z histone variants facilitate HDACi-dependent removal of H3.3K27M mutant protein in pediatric high-grade glioma cells.Cell reports · 2024Article
- Identification of a chemoresistance-related prognostic gene signature by comprehensive analysis and experimental validation in pancreatic cancer.Frontiers in oncology · 2023Article
- Genomics and Epigenomics in the Molecular Biology of Melanoma-A Prerequisite for Biomarkers Studies.International journal of molecular sciences · 2022Review
- Epigenetics, DNA damage, and aging.The Journal of clinical investigation · 2022Review
- E2F and STAT3 provide transcriptional synergy for histone variant H2AZ activation to sustain glioblastoma chromatin accessibility and tumorigenicity.Cell death and differentiation · 2022Article
- MALDI Mass Spectrometry Imaging for the Distinction of Adenocarcinomas of the Pancreas and Biliary Tree.Molecules (Basel, Switzerland) · 2022Article
Corrections and comments
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Authors and funding
15 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is one of the most intractable and devastating malignant tumors. Epigenetic modifications such as DNA methylation and histone modification regulate tumor initiation and progression. However, the contribution of histone variants in PDAC is unknown. Here, we demonstrated that the histone variant H2A.Z is highly expressed in PDAC cell lines and PDAC patients and that its overexpression correlates with poor prognosis. Moreover, all three H2A.Z isoforms (H2A.Z.1, H2A.Z.2.1, and H2A.Z.2.2) are highly expressed in PDAC cell lines and PDAC patients. Knockdown of these H2A.Z isoforms in PDAC cell lines induces a senescent phenotype, cell cycle arrest in phase G2/M, increased expression of cyclin-dependent kinase inhibitor CDKN2A/p16, SA-β-galactosidase activity and interleukin 8 production. Transcriptome analysis of H2A.Z-depleted PDAC cells showed altered gene expression in fatty acid biosynthesis pathways and those that regulate cell cycle and DNA damage repair. Importantly, depletion of H2A.Z isoforms reduces the tumor size in a mouse xenograft model in vivo and sensitizes PDAC cells to gemcitabine. Overexpression of H2A.Z.1 and H2A.Z.2.1 more than H2A.Z.2.2 partially restores the oncogenic phenotype. Therefore, our data suggest that overexpression of H2A.Z isoforms enables cells to overcome the oncoprotective barrier associated with senescence, favoring PDAC tumor grow and chemoresistance. These results make H2A.Z a potential candidate as a diagnostic biomarker and therapeutic target for PDAC.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.