ArticleCell cycle (Georgetown, Tex.)2013
JNK and STAT3 signaling pathways converge on Akt-mediated phosphorylation of EZH2 in bronchial epithelial cells induced by arsenic.
Article in Cell cycle (Georgetown, Tex.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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40 citing papers in PubMed, 76 citations in OpenAlex.
- Inhibition of STAT3-mediated glycolysis by bruceine D suppresses non-small-cell lung cancer progressionCancer biology & therapy · 2026Article
- Arsenic disrupts H3K9me3 and H3K27me3 balance by biasing PRC2.1 and PRC2.2 activity via PALI1 inhibition in carcinogenesis.International journal of biological sciences · 2025Article
- Morphological Changes Induced by TKS4 Deficiency Can Be Reversed by EZH2 Inhibition in Colorectal Carcinoma Cells.Biomolecules · 2024Article
- The roles of EZH2 in cancer and its inhibitors.Medical oncology (Northwood, London, England) · 2023Review
- Arsenic and cancer: Evidence and mechanisms.Advances in pharmacology (San Diego, Calif.) · 2023Article
- Arsenic activates STAT3 signaling during the transformation of the human bronchial epithelial cells.Toxicology and applied pharmacology · 2022Article
- The unfavorable clinical outcome of COVID-19 in smokers is mediated by H3K4me3, H3K9me3 and H3K27me3 histone marks.Epigenomics · 2022Review
- Epigenetics and environment in breast cancer: New paradigms for anti-cancer therapies.Frontiers in oncology · 2022Review
- Integration of Epigenetic Mechanisms into Non-Genotoxic Carcinogenicity Hazard Assessment: Focus on DNA Methylation and Histone Modifications.International journal of molecular sciences · 2021Review
- Going beyond Polycomb: EZH2 functions in prostate cancer.Oncogene · 2021Review
- The Prognostic Significance of Anisomycin-Activated Phospho-c-Jun NH2-Terminal Kinase (p-JNK) in Predicting Breast Cancer Patients' Survival Time.Frontiers in cell and developmental biology · 2021Article
- The Pivotal Immunomodulatory and Anti-Inflammatory Effect of Histone-Lysine N-Methyltransferase in the Glioma Microenvironment: Its Biomarker and Therapy Potentials.Analytical cellular pathology (Amsterdam) · 2021Review
- Post-translational modifications of EZH2 in cancer.Cell & bioscience · 2020Review
- Chronic and acute arsenic exposure enhance EGFR expression via distinct molecular mechanisms.Toxicology in vitro : an international journal published in association with BIBRA · 2020Article
- TCDD-mediated suppression of naïve human B cell IgM secretion involves aryl hydrocarbon receptor-mediated reduction in STAT3 serine 727 phosphorylation and is restored by interferon-γ.Cellular signalling · 2020Article
- Metal carcinogen exposure induces cancer stem cell-like property through epigenetic reprograming: A novel mechanism of metal carcinogenesis.Seminars in cancer biology · 2019Review
- Metabolic and epigenetic reprogramming in the arsenic-induced cancer stem cells.Seminars in cancer biology · 2019Review
- The Attenuation of Trophoblast Invasion Caused by the Downregulation of EZH2 Is Involved in the Pathogenesis of Human Recurrent Miscarriage.Molecular therapy. Nucleic acids · 2019Article
- STAT3 enhances the constitutive activity of AGC kinases in melanoma by transactivating PDK1.Cell & bioscience · 2019Article
- PARP-1 overexpression contributes to Cadmium-induced death in rat proximal tubular cells via parthanatos and the MAPK signalling pathway.Scientific reports · 2017Article
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6 authors at 1 institution in 2 countries.
Funding
Abstract
The molecular mechanisms by which arsenic (As ( 3+) ) causes human cancers remain to be fully elucidated. Enhancer of zeste homolog 2 (EZH2) is the catalytic subunit of polycomb-repressive complexes 2 (PRC2) that promotes trimethylation of lysine 27 of histone H3, leading to altered expression of tumor suppressors or oncogenes. In the present study, we determined the effect of As ( 3+) on EZH2 phosphorylation and the signaling pathways important for As ( 3+) -induced EZH2 phosphorylation in human bronchial epithelial cell line BEAS-2B. The involvement of kinases in As ( 3+) -induced EZH2 phosphorylation was validated by siRNA-based gene silencing. The data showed that As ( 3+) can induce phosphorylation of EZH2 at serine 21 in human bronchial epithelial cells and that the phosphorylation of EZH2 requires an As ( 3+) -activated signaling cascade from JNK and STAT3 to Akt. Transfection of the cells with siRNA specific for JNK1 revealed that JNK silencing reduced serine727 phosphorylation of STAT3, Akt activation and EZH2 phosphorylation, suggesting that JNK is the upstream kinase involved in As ( 3+) -induced EZH2 phosphorylation. Because As ( 3+) is capable of inducing miRNA-21 (miR-21), a STAT3-regulated miRNA that represses protein translation of PTEN or Spry2, we also tested the role of STAT3 and miR-21 in As ( 3+) -induced EZH2 phosphorylation. Ectopic overexpression of miR-21 promoted Akt activation and phosphorylation of EZH2, whereas inhibiting miR-21 by transfecting the cells with anti-miR-21 inhibited Akt activation and EZH2 phosphorylation. Taken together, these results demonstrate a contribution of the JNK, STAT3 and Akt signaling axis to As ( 3+) -induced EZH2 phosphorylation. Importantly, these findings may reveal new molecular mechanisms underlying As ( 3+) -induced carcinogenesis.
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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.