期刊
ONCOGENE
卷 32, 期 14, 页码 1811-1820出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/onc.2012.197
关键词
AhR; cell plasticity; FAK; integrin; Src
资金
- ANSES (Agence Nationale de SEcurite Sanitaire de l'alimentation, de l'environnement et du travail)
- ANR (Agence Nationale de la Recherche) [06SEST26]
- ARC (Association pour la Recherche sur le Cancer) [3927, SFI20101201842]
- CNRS (Center Nationale de la recherche scientifique)
- Fondation pour la Recherche Medicale
- Ecole Doctorale du Medicament
- Hospitals Europeen Georges Pompidou and Necker Enfants Malade
- INSERM (Institut National de la Sante et de la Recherche Medicale)
- Ligue contre le Cancer
- Ministere de l'enseignement superieur et de la recherche
- Region Ile de France
- Universite Paris Descartes, Paris Sorbonne Cite
The aryl hydrocarbon receptor (AhR) is commonly described as a transcription factor, which regulates xenobiotic-metabolizing enzymes. Recent studies have suggested that the binding of ligands to the AhR also activates the Src kinase. In this manuscript, we show that the AhR, through the activation of Src, activates focal adhesion kinase (FAK) and promotes integrin clustering. These effects contribute to cell migration. Further, we show that the activation of the AhR increases the interaction of FAK with the metastatic marker, HEF1/NEDD9/CAS-L, and the expression of several integrins. Xenobiotic exposure, thus, may contribute to novel cell-migratory programs. Oncogene (2013) 32, 1811-1820; doi: 10.1038/onc.2012.197; published online 4 June 2012
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