ArticleJournal of cellular physiology2009
Soluble and insoluble nickel compounds exert a differential inhibitory effect on cell growth through IKKalpha-dependent cyclin D1 down-regulation.
Article in Journal of cellular physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 27 citations in OpenAlex.
- Contaminant Metals and Cardiovascular Health.Journal of cardiovascular development and disease · 2023Review
- Among Gerontogens, Heavy Metals Are a Class of Their Own: A Review of the Evidence for Cellular Senescence.Brain sciences · 2023Review
- Nickel carcinogenesis mechanism: cell cycle dysregulation.Environmental science and pollution research international · 2021Review
- Metal nickel exposure increase the risk of congenital heart defects occurrence in offspring: A case-control study in China.Medicine · 2019Article
- Decreased c-Myc mRNA Stability via the MicroRNA 141-3p/AUF1 Axis Is Crucial for p63α Inhibition of Cyclin D1 Gene Transcription and Bladder Cancer Cell Tumorigenicity.Molecular and cellular biology · 2018Article
- Article
- 10th NTES Conference: Nickel and Arsenic Compounds Alter the Epigenome of Peripheral Blood Mononuclear Cells.Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS) · 2015Article
- A new tumour suppression mechanism by p27Kip1: EGFR down-regulation mediated by JNK/c-Jun pathway inhibition.The Biochemical journal · 2014Article
- Effect of nickel chloride on cell proliferation.The open dentistry journal · 2012Article
- E3 ligase activity of XIAP RING domain is required for XIAP-mediated cancer cell migration, but not for its RhoGDI binding activity.PloS one · 2012Article
- The role of cadmium and nickel in estrogen receptor signaling and breast cancer: metalloestrogens or not?Journal of environmental science and health. Part C, Environmental carcinogenesis & ecotoxicology reviews · 2012Review
- Nickel-induced down-regulation of ΔNp63 and its role in the proliferation of keratinocytes.Toxicology and applied pharmacology · 2011Article
- A cross-talk between NFAT and NF-κB pathways is crucial for nickel-induced COX-2 expression in Beas-2B cells.Current cancer drug targets · 2011Article
- X-linked inhibitor of apoptosis protein (XIAP) mediates cancer cell motility via Rho GDP dissociation inhibitor (RhoGDI)-dependent regulation of the cytoskeleton.The Journal of biological chemistry · 2011Article
- Reactive oxygen species-activated Akt/ASK1/p38 signaling pathway in nickel compound-induced apoptosis in BEAS 2B cells.Chemical research in toxicology · 2010Article
- A novel role of IKKalpha in the mediation of UVB-induced G0/G1 cell cycle arrest response by suppressing Cyclin D1 expression.Biochimica et biophysica acta · 2010Article
- A genome-wide deletion mutant screen identifies pathways affected by nickel sulfate in Saccharomyces cerevisiae.BMC genomics · 2009Article
- Effects of nickel on cyclin expression, cell cycle progression and cell proliferation in human pulmonary cells.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2009Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
It is well-known that insoluble nickel compounds possess much more potent carcinogenic activities as compared with soluble nickel compounds. Although it is assumed that the different entry and clearance rate are responsible for the difference, the mechanisms underlying the different carcinogenic activities are still not well understood yet. In the present study, we found that exposure to soluble, but not insoluble nickel compounds, caused a significant inhibition of cell growth and G1/G0 cell cycle arrest, which was concomitant with a marked down-regulation of cylin D1, an essential nuclear protein for controlling G1/S transition, while both soluble and insoluble nickel compounds showed similar effects on NFkappaB activation, HIF-1alpha protein accumulation and TNF-alpha transcription and CAP43 protein expression at same doses range. The down-regulation of cyclin D1 is due to protein degradation rather than inhibition of transcription, because the nickel compounds treatment did not change cyclin D1 mRNA level, while MG132, the proteasome inhibitor, can rescue the degradation of cyclin D1 caused by soluble nickel compound. Moreover, the soluble nickel-induced cyclin D1 degradation is dependent on its Thr286 residue and requires IKKalpha, but not HIF-1alpha, which are both reported to be involved in cyclin D1 down-regulation. Taken together, we demonstrate that soluble, but not insoluble nickel compound, is able to cause cyclin D1 degradation and a cell growth arrest in an IKKalpha-dependent manner. Given the role of cyclin D1 and cell proliferation in carcinogenesis, we anticipate that the different effects of soluble and insoluble nickel compounds on cyclin D1 degradation and cell growth arrest may at least partially account for their different carcinogenic activities.
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