ArticleEBioMedicine2017
Histone Chaperone ASF1A Predicts Poor Outcomes for Patients With Gastrointestinal Cancer and Drives Cancer Progression by Stimulating Transcription of β-Catenin Target Genes.
Article in EBioMedicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed.
- ASF1A: A versatile histone chaperone bridging chromatin dynamics, disease mechanisms and clinical potential (Review).Experimental and therapeutic medicine · 2026Review
- Article
- Characterizing the salivary RNA landscape to identify potential diagnostic, prognostic, and follow-up biomarkers for breast cancer.Molecular oncology · 2026Article
- A novel telomere-associated genes signature for the prediction of prognosis and treatment responsiveness of hepatocellular carcinoma.Biological procedures online · 2025Article
- Novel Copy Number Deletion InvolvingClinical case reports · 2025Article
- ASF1A-dependent P300-mediated histone H3 lysine 18 lactylation promotes atherosclerosis by regulating EndMT.Acta pharmaceutica Sinica. B · 2024Article
- Comparative Review on Cancer Pathology from Aberrant Histone Chaperone Activity.International journal of molecular sciences · 2024Review
- Unnatural helical peptidic foldamers as protein segment mimics.Chemical Society reviews · 2023Review
- Construction and Validation of a Protein-associated Prognostic Model for Gastrointestinal Cancer.Combinatorial chemistry & high throughput screening · 2023Article
- Review
- Histone chaperone ASF1A accelerates chronic myeloid leukemia blast crisis by activating Notch signaling.Cell death & disease · 2022Article
- Screening a novel six critical gene-based system of diagnostic and prognostic biomarkers in prostate adenocarcinoma patients with different clinical variables.American journal of translational research · 2022Article
- Optimal anchoring of a foldamer inhibitor of ASF1 histone chaperone through backbone plasticity.Science advances · 2021Article
- Chk1 promotes non-homologous end joining in G1 through direct phosphorylation of ASF1A.Cell reports · 2021Article
- Oncogenic herpesvirus KSHV triggers hallmarks of alternative lengthening of telomeres.Nature communications · 2021Article
- Epigenetics in prostate cancer treatment.Journal of translational genetics and genomics · 2021Article
- Telomere-related Markers for Cancer.Current topics in medicinal chemistry · 2020Review
- ASF1a inhibition induces p53-dependent growth arrest and senescence of cancer cells.Cell death & disease · 2019Article
- CHAF1A interacts with TCF4 to promote gastric carcinogenesis via upregulation of c-MYC and CCND1 expression.EBioMedicine · 2018Article
- Oncogenic potential of CHAF1A in gastric cancer: A novel link with Helicobacter pylori-driven carcinogenesis?EBioMedicine · 2018Article
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12 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Epigenetic mechanisms play a key role in gastrointestinal cancer (GIC) development and progression, and most studies have been focused on aberrant DNA methylation and histone modifying enzymes. However, the histone H3-H4 chaperone ASF1A is an important factor regulating chromatin assembling and gene transcription, while it is currently unclear whether ASF1A is involved in cancer pathogenesis. The present study is thus designed to address this issue. Here we showed that ASF1A expression was widespread in GIC-derived cell lines and up-regulated in primary GIC. Higher levels of ASF1A expression predicted significantly shorter patient overall survival in colorectal cancer (P=0.0012). The further analyses of the GEO dataset validate higher ASF1A expression as a prognostic factor for CRC patients. Mechanistically, ASF1A interacted with β-catenin and promoted the transcription of β-catenin target genes including c-MYC, cyclin D1, ZEB1 and LGR5, thereby stimulating proliferation, stemness and migration/invasion of GIC cells. β-Catenin inhibition abolished these effects of ASF1A. Moreover, the ASF1A-β-catenin-ZEB1 axis down-regulated E-Cadherin expression, thereby contributing to enhanced migration/invasion of GIC cells. ASF1A over-expression and depletion facilitated and inhibited in vivo tumor growth and/or metastasis in mouse xenograft models, respectively. Taken together, ASF1A is aberrantly over-expressed in GIC tumors and plays key roles in GIC development and progression by stimulating the transcription of β-catenin target genes. ASF1A may thus be a novel target for GIC therapy and a potential prognostic marker.
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