ArticleCarcinogenesis2010
Hypoxia and nickel inhibit histone demethylase JMJD1A and repress Spry2 expression in human bronchial epithelial BEAS-2B cells.
Article in Carcinogenesis, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 94 citations in OpenAlex.
- Metal carcinogens and cancer: integrating genetic and epigenetic perspectives.Frontiers in oncology · 2026Review
- Investigating Hippocampal Lateralization: Effects of Nickel on Neurobiological, AchE Activity, and Neurobehavioral Changes in the Wistar Rats.Molecular neurobiology · 2025Article
- Metabolomics: a promising tool for deciphering metabolic impairment in heavy metal toxicities.Frontiers in molecular biosciences · 2023Review
- Review
- Epigenetic Regulation in Exposome-Induced Tumorigenesis: Emerging Roles of ncRNAs.Biomolecules · 2022Review
- Redox sensitive miR-27a/b/Nrf2 signaling in Cr(VI)-induced carcinogenesis.The Science of the total environment · 2022Article
- Epigenetic mechanisms in metal carcinogenesis.Toxicology reports · 2022Review
- Integrative Bioinformatics approaches to therapeutic gene target selection in various cancers for Nitroglycerin.Scientific reports · 2021Article
- Epithelial-mesenchymal transition: Insights into nickel-induced lung diseases.Seminars in cancer biology · 2021Review
- Integration of Epigenetic Mechanisms into Non-Genotoxic Carcinogenicity Hazard Assessment: Focus on DNA Methylation and Histone Modifications.International journal of molecular sciences · 2021Review
- Role of Epigenetics in the Pathogenesis, Treatment, Prediction, and Cellular Transformation of Asthma.Mediators of inflammation · 2021Review
- Update of the risk assessment of nickel in food and drinking water.EFSA journal. European Food Safety Authority · 2020Article
- Review
- Melatonin Antagonizes Nickel-Induced Aerobic Glycolysis by Blocking ROS-Mediated HIF-1Oxidative medicine and cellular longevity · 2020Article
- Nickel-induced transcriptional changes persist post exposure through epigenetic reprogramming.Epigenetics & chromatin · 2019Article
- Metals and Mechanisms of Carcinogenesis.Annual review of pharmacology and toxicology · 2019Review
- Small molecule KDM4s inhibitors as anti-cancer agents.Journal of enzyme inhibition and medicinal chemistry · 2018Article
- Tungsten exposure causes a selective loss of histone demethylase protein.Molecular carcinogenesis · 2017Article
- A Tox21 Approach to Altered Epigenetic Landscapes: Assessing Epigenetic Toxicity Pathways Leading to Altered Gene Expression and Oncogenic Transformation In Vitro.International journal of molecular sciences · 2017Review
- Nickel induces transcriptional down-regulation of DNA repair pathways in tumorigenic and non-tumorigenic lung cells.Carcinogenesis · 2017Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Epigenetic silencing of tumor suppressor genes commonly occurs in human cancers via increasing DNA methylation and repressive histone modifications at gene promoters. However, little is known about how pathogenic environmental factors contribute to cancer development by affecting epigenetic regulatory mechanisms. Previously, we reported that both hypoxia and nickel (an environmental carcinogen) increased global histone H3 lysine 9 methylation in cells through inhibiting a novel class of iron- and α-ketoglutarate-dependent histone demethylases. Here, we investigated whether inhibition of histone demethylase JMJD1A by hypoxia and nickel could lead to repression/silencing of JMJD1A-targeted gene(s). By using Affymetrix GeneChip and ChIP-on-chip technologies, we identified Spry2 gene, a key regulator of receptor tyrosine kinase/extracellular signal-regulated kinase (ERK) signaling, as one of the JMJD1A-targeted genes in human bronchial epithelial BEAS-2B cells. Both hypoxia and nickel exposure increased the level of H3K9me2 at the Spry2 promoter by inhibiting JMJD1A, which probably led to a decreased expression of Spry2 in BEAS-2B cells. Repression of Spry2 potentiated the nickel-induced ERK phosphorylation, and forced expression of Spry2 in BEAS-2B cells decreased the nickel-induced ERK phosphorylation and significantly suppressed nickel-induced anchorage-independent growth. Taken together, our results suggest that histone demethylases could be targets of environmental carcinogens and their inhibition may lead to altered gene expression and eventually carcinogenesis.
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Registered trials
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.