ArticleCancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology2009
Effects of nickel on cyclin expression, cell cycle progression and cell proliferation in human pulmonary cells.
Article in Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 51 citations in OpenAlex.
- A comprehensive examination of the impact of environmental pollution on lung cancer: A review.Journal of advanced research · 2026Review
- The Protective Effects of Methionine on Nickel-Induced Oxidative Stress via NF-κB Pathway in the Kidneys of Mice.Biological trace element research · 2025Article
- Unveiling the Toxicity of Fine and Nano-Sized Airborne Particles Generated from Industrial Thermal Spraying Processes in Human Alveolar Epithelial Cells.International journal of molecular sciences · 2022Article
- Cellular and Molecular Signatures of Oxidative Stress in Bronchial Epithelial Cell Models Injured by Cigarette Smoke Extract.International journal of molecular sciences · 2022Review
- Protection of lead-induced cytotoxicity using paramagnetic nickel-insulin quantum clusters.RSC advances · 2021Article
- Nickel chloride administration prevents the growth of oral squamous cell carcinoma.Oncotarget · 2018Article
- Nickel and cadmium-induced SLBP depletion: A potential pathway to metal mediated cellular transformation.PloS one · 2017Article
- Downregulated long non-coding RNA CLMAT3 promotes the proliferation of colorectal cancer cells by targeting regulators of the cell cycle pathway.Oncotarget · 2016Article
- Repeated PM2.5 exposure inhibits BEAS-2B cell P53 expression through ROS-Akt-DNMT3B pathway-mediated promoter hypermethylation.Oncotarget · 2016Article
- Proteomic Assessment of Biochemical Pathways That Are Critical to Nickel-Induced Toxicity Responses in Human Epithelial Cells.PloS one · 2016Article
- Article
- Culture conditions profoundly impact phenotype in BEAS-2B, a human pulmonary epithelial model.Journal of applied toxicology : JAT · 2015Article
- Disruptive chemicals, senescence and immortality.Carcinogenesis · 2015Review
- ψ-Bufarenogin, a novel anti-tumor compound, suppresses liver cancer growth by inhibiting receptor tyrosine kinase-mediated signaling.Oncotarget · 2015Article
- Molecular basis of arsenite (As⁺³)-induced acute cytotoxicity in human cervical epithelial carcinoma cells.The Libyan journal of medicine · 2015Article
- Textile industry manufacturing by-products induce human melanoma cell proliferation via ERK1/2 activation.Cell proliferation · 2014Article
- Toxicogenomic effect of nickel and beyond.Archives of toxicology · 2014Review
- Cell cycle alterations induced by urban PM2.5 in bronchial epithelial cells: characterization of the process and possible mechanisms involved.Particle and fibre toxicology · 2013Article
- Anti-apoptotic proteins and catalase-dependent apoptosis resistance in nickel chloride-transformed human lung epithelial cells.International journal of oncology · 2013Article
- p53 activation by Ni(II) is a HIF-1α independent response causing caspases 9/3-mediated apoptosis in human lung cells.Toxicology and applied pharmacology · 2013Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
Frequent exposure to nickel compounds has been considered as one of the potential causes of human lung cancer. However, the molecular mechanism of nickel-induced lung carcinogenesis remains obscure. In the current study, slight S-phase increase, significant G(2)/M cell cycle arrest, and proliferation blockage were observed in human bronchial epithelial cells (Beas-2B) upon nickel exposure. Moreover, the induction of cyclin D1 and cyclin E by nickel was shown for the first time in human pulmonary cells, which may be involved in nickel-triggered G(1)/S transition and cell transformation. In addition, we verified that hypoxia-inducible factor-1alpha, an important transcription factor of nickel response, was not required for the cyclin D1 or cyclin E induction. The role of p53 in nickel-induced G(2)/M arrest was excluded, respecting that its protein level, ser(15) phosphorylation, and transcriptional activity were not changed in nickel response. Further study revealed that cyclin A was not activated in nickel response, and cyclin B1, which not only promotes G(2)/M transition but also prevents M-phase exit of cells if not degraded in time, was up-regulated by nickel through a manner independent of hypoxia-inducible factor. More importantly, our results verified that overexpressed cyclin B1, veiling the effect of cyclin D1 or cyclin E, mediated nickel-caused M-phase blockage and cell growth inhibition, which may render pulmonary cells more sensitive to DNA damage and facilitates cancer initiation. These results will not only deepen our understanding of the molecular mechanism involved in nickel carcinogenecity, but also lead to the further study on chemoprevention of nickel-associated human cancer.
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