ArticleOncogene2004
Src-dependent ERK5 and Src/EGFR-dependent ERK1/2 activation is required for cell proliferation by asbestos.
Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
29 citing papers in PubMed, 90 citations in OpenAlex.
- Review
- Do Carbon Nanotubes and Asbestos Fibers Exhibit Common Toxicity Mechanisms?Nanomaterials (Basel, Switzerland) · 2022Review
- Targeting MAPK Signaling in Age-Related Macular Degeneration.Ophthalmology and eye diseases · 2016Review
- ERK5 negatively regulates tobacco smoke-induced pulmonary epithelial-mesenchymal transition.Oncotarget · 2015Article
- Activation of Proinflammatory Responses in Cells of the Airway Mucosa by Particulate Matter: Oxidant- and Non-Oxidant-Mediated Triggering Mechanisms.Biomolecules · 2015Review
- Indications for distinct pathogenic mechanisms of asbestos and silica through gene expression profiling of the response of lung epithelial cells.Human molecular genetics · 2015Article
- Extracellular signal-regulated kinase 5 and cyclic AMP response element binding protein are novel pathways inhibited by vandetanib (ZD6474) and doxorubicin in mesotheliomas.American journal of respiratory cell and molecular biology · 2014Article
- Down regulation of RhoC by microRNA-138 results in de-activation of FAK, Src and Erk1/2 signaling pathway in head and neck squamous cell carcinoma.Oral oncology · 2014Article
- ERK5/KLF4 signaling as a common mediator of the neuroprotective effects of both nerve growth factor and hydrogen peroxide preconditioning.Age (Dordrecht, Netherlands) · 2014Article
- Extracellular signal-regulated kinase 5: a potential therapeutic target for malignant mesotheliomas.Clinical cancer research : an official journal of the American Association for Cancer Research · 2013Article
- Cigarette smoke extract stimulates epithelial-mesenchymal transition through Src activation.Free radical biology & medicine · 2012Article
- MEK5/ERK5 pathway: the first fifteen years.Biochimica et biophysica acta · 2012Review
- ERK2 is essential for the growth of human epithelioid malignant mesotheliomas.International journal of cancer · 2011Article
- Targeting the BMK1 MAP kinase pathway in cancer therapy.Clinical cancer research : an official journal of the American Association for Cancer Research · 2011Article
- Apoptotic cell-derived factors induce arginase II expression in murine macrophages by activating ERK5/CREB.Cellular and molecular life sciences : CMLS · 2011Article
- Article
- Asbestos, lung cancers, and mesotheliomas: from molecular approaches to targeting tumor survival pathways.American journal of respiratory cell and molecular biology · 2010Review
- Extracellular signal regulated kinase 5 mediates signals triggered by the novel tumor promoter palytoxin.Toxicology and applied pharmacology · 2009Article
- A protein kinase Cdelta-dependent protein kinase D pathway modulates ERK1/2 and JNK1/2 phosphorylation and Bim-associated apoptosis by asbestos.The American journal of pathology · 2009Article
- Analysis of the impact of ERK5, JNK, and P38 kinase cascades on each other: a systems approach.Bioinformation · 2009Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Crocidolite asbestos elicits oxidative stress and cell proliferation, but the signaling cascades linked to these outcomes are unclear. To determine the role of mitogen-activated protein kinases (MAPK) in asbestos-induced cell signaling, we evaluated the effects of crocidolite asbestos, EGF and H2O2, on MAPK activation in murine lung epithelial cells (C10 line). In contrast to rapid and transient activation of extracellular signal-regulated kinase 5 (ERK5) by EGF or H2O2, asbestos caused protracted oxidant-dependent ERK5 activation that was inhibited by an Src kinase inhibitor (PP2), but not by an inhibitor of epidermal growth factor receptor (EGFR) phosphorylation (AG1478). ERK1/2 activation by asbestos was inhibited by either PP2 or AG1478. To confirm the involvement of Src in ERK1/2 and ERK5 activation, a dominant-negative Src construct was used. These experiments showed that Src was essential for ERK1/2 and also ERK5 phosphorylation by asbestos. Time frame studies indicated immediate activation of Src by asbestos fibers, whereas EGFR phosphorylation occurred subsequently. Data suggest that asbestos causes activation of ERK5 through an EGFR-independent pathway, whereas ERK1/2 activation is dependent on Src through a mechanism involving phosphorylation of the EGFR. Furthermore, Src, ERK1/2 and ERK5 activation are essential for cell proliferation by asbestos. The use of a dominant-negative ERK5 construct caused selective downregulation of c-jun expression, whereas inhibition of Src by PP2 or MEK1 by PD98059 caused decreases in c-fos, fra-1 and c-jun expression in asbestos-exposed C10 cells. These observations may have broad relevance to cell proliferation by carcinogenic mineral fibers and oxidants.
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Registered trials
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