ArticlePloS one2016
Hexavalent Chromium (Cr(VI)) Down-Regulates Acetylation of Histone H4 at Lysine 16 through Induction of Stressor Protein Nupr1.
Article in PloS one, 2016. 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, 50 citations in OpenAlex.
- KAT8-mediated epigenetic modifications: Physiological functions, heterogeneity in disease, and advances in targeted development.iScience · 2026Review
- MGMT, NUPR1, NDRG2, and GLI1 Gene Promoter Methylation in Glioblastoma Tissues and Association with Clinical Characteristics and Therapeutic Outcomes.International journal of molecular sciences · 2026Article
- Epigenetic mechanisms linking hexavalent chromium exposure to pancreatic cancer risk: a systematic review.Environmental epigenetics · 2026Review
- Trivalent chromium interacts directly with acetylated lysine.Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS) · 2025Article
- Lysine Acetyltransferase 8: A Target for Natural Compounds in Cancer Therapy.International journal of molecular sciences · 2025Review
- Carcinogenic Mechanisms of Hexavalent Chromium: From DNA Breaks to Chromosome Instability and Neoplastic Transformation.Current environmental health reports · 2024Review
- Chromate Affects Gene Expression and DNA Methylation in Long-Term In Vitro Experiments in A549 Cells.International journal of molecular sciences · 2024Article
- NUPR1 packaged in extracellular vesicles promotes murine triple-negative breast cancer in a type 1 interferon-independent manner.Extracellular vesicles and circulating nucleic acids · 2024Article
- Epigenetic and epitranscriptomic mechanisms of chromium carcinogenesis.Advances in pharmacology (San Diego, Calif.) · 2023Article
- Review
- Epigenetic Regulation in Exposome-Induced Tumorigenesis: Emerging Roles of ncRNAs.Biomolecules · 2022Review
- Current understanding of hexavalent chromium [Cr(VI)] neurotoxicity and new perspectives.Environment international · 2022Review
- Hexavalent chromium promotes differential binding of CTCF to its cognate sites in Euchromatin.Epigenetics · 2021Article
- Hexavalent chromium disrupts chromatin architecture.Seminars in cancer biology · 2021Review
- CircRNA HIPK3 promotes the progression of oral squamous cell carcinoma through upregulation of the NUPR1/PI3K/AKT pathway by sponging miR-637.Annals of translational medicine · 2021Article
- Induction of NUPR1 and AP‑1 contributes to the carcinogenic potential of nickel.Oncology reports · 2021Article
- Nuclear protein 1 imparts oncogenic potential and chemotherapeutic resistance in cancer.Cancer letters · 2020Review
- Molecular and epigenetic mechanisms of Cr(VI)-induced carcinogenesis.Toxicology and applied pharmacology · 2019Review
- Chromium exposure disrupts chromatin architecture upsetting the mechanisms that regulate transcription.Experimental biology and medicine (Maywood, N.J.) · 2019Review
- Mechanisms of Chromium-Induced Toxicity.Current opinion in toxicology · 2019Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
The environmental and occupational carcinogen Hexavalent Chromium (Cr(VI)) has been shown to cause lung cancer in humans when inhaled. In spite of a considerable research effort, the mechanisms of Cr(VI)-induced carcinogenesis remain largely unknown. Nupr1 (nuclear protein 1) is a small, highly basic, and unfolded protein with molecular weight of 8,800 daltons and is induced by a variety of stressors. Studies in animal models have suggested that Nupr1 is a key factor in the development of lung and pancreatic cancers, with little known about the underlying molecular mechanisms. Here we report that the level of Nupr1 is significantly increased in human bronchial epithelial BEAS2B cells following exposure to Cr(VI) through epigenetic mechanisms. Interestingly, Cr(VI) exposure also results in the loss of acetylation at histone H4K16, which is considered a 'hallmark' of human cancer. Cr(VI)-induced reduction of H4K16 acetylation appears to be caused by the induction of Nupr1, since (a) overexpression of Nupr1 decreased the levels of both H4K16 acetylation and the histone acetyltransferase MOF (male absent on the first; also known as Kat8, Myst 1), which specifically acetylates H4K16; (b) the loss of acetylation of H4K16 upon Cr(VI) exposure is greatly compromised by knockdown of Nupr1. Moreover, Nupr1-induced reduction of H4K16 acetylation correlates with the transcriptional down-regulation at several genomic loci. Notably, overexpression of Nupr1 induces anchorage-independent cell growth and knockdown of Nupr1 expression prevents Cr(VI)-induced cell transformation. We propose that Cr(VI) induces Nupr1 and rapidly perturbs gene expression by downregulating H4K16 acetylation, thereby contributing to Cr(VI)-induced carcinogenesis.
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