ArticleMolecular cancer2007
Fra-1 governs cell migration via modulation of CD44 expression in human mesotheliomas.
Article in Molecular cancer, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- Construction of multifunctional hydrogel with metal-polyphenol capsules for infected full-thickness skin wound healing.Bioactive materials · 2023Article
- Dihydroartemisinin beneficially regulates splenic immune cell heterogeneity through the SOD3-JNK-AP-1 axis.Science China. Life sciences · 2022Article
- Expression and function of FRA1 protein in tumors.Molecular biology reports · 2020Review
- miR-497 suppresses epithelial-mesenchymal transition and metastasis in colorectal cancer cells by targeting fos-related antigen-1.OncoTargets and therapy · 2016Article
- Fra-1 is a key driver of colon cancer metastasis and a Fra-1 classifier predicts disease-free survival.Oncotarget · 2015Article
- Reactive oxygen species a double-edged sword for mesothelioma.Oncotarget · 2015Review
- Exemestane blocks mesothelioma growth through downregulation of cAMP, pCREB and CD44 implicating new treatment option in patients affected by this disease.Molecular cancer · 2014Article
- New insights into understanding the mechanisms, pathogenesis, and management of malignant mesotheliomas.The American journal of pathology · 2013Review
- Article
- Estrogen-induced expression of Fos-related antigen 1 (FRA-1) regulates uterine stromal differentiation and remodeling.The Journal of biological chemistry · 2012Article
- Suppression of AP1 transcription factor function in keratinocyte suppresses differentiation.PloS one · 2012Article
- Cell specific CD44 expression in breast cancer requires the interaction of AP-1 and NFκB with a novel cis-element.PloS one · 2012Article
- Osteopontin modulates inflammation, mucin production, and gene expression signatures after inhalation of asbestos in a murine model of fibrosis.The American journal of pathology · 2011Article
- c-Jun-NH2 terminal kinase (JNK)-mediates AP-1 activation by thioredoxin: phosphorylation of cJun, JunB, and Fra-1.Molecular and cellular biochemistry · 2010Article
- Asbestos, lung cancers, and mesotheliomas: from molecular approaches to targeting tumor survival pathways.American journal of respiratory cell and molecular biology · 2010Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Silencing of Fra-1, a component of the dimeric transcription factor, activator protein-1 (AP-1), inhibits mRNA expression of c-met and cd44 in rat mesothelioma cells and is causally linked to maintenance of the transformed phenotype. However, the mechanisms of Fra-1 regulation and Fra-1 regulated gene expression in human malignant mesothelioma (MM) are unclear. We first show in a panel of human MM cells that Fra-1 mRNA expression in MM is complex and regulated by extracellular signal-regulated kinase (ERK1, ERK2), Src, and phosphatidyl-inositol-3-kinase (PI3K) pathways in a tumor-specific fashion. Cell lines with PI3K-dependent Fra-1 expression were SV40 positive and expressed the lowest basal Fra-1 levels. Levels of Fra-1 expression correlated with amounts of CD44 expression that were greater in simian virus 40 negative (SV40-) MM cells. Using dominant negative (dn), short hairpin (sh) and small interference (si) RNA constructs, we next demonstrate that expression of CD44, the principal hyaluronic receptor in MMs, correlates with Fra-expression in both simian virus 40 positive (SV40+) and SV40- MMs. Moreover, both Fra-1 and CD44 expression are linked to cell migration in SV40- MM cells. Lastly, in contrast to normal lung tissue, tissue microarrays revealed that Fra-1 was expressed in 33 of 34 human MMs, and that all CD44+ tumors were SV40-. These results suggest that Fra-1 is associated with cell migration in human MMs and that Fra-1 modulation of CD44 may govern migration of selected MMs.
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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.