The tobacco-specific carcinogen-operated calcium channel promotes lung tumorigenesis via IGF2 exocytosis in lung epithelial cells

The binding of tobacco-specific carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) to nicotinic acetylcholine receptors (nAChRs) induces calcium signalling. Here the authors show that NKK-induced calcium influx in airway epithelial cells triggers IGF2 secretion and tumourigenesis.

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Detalles Bibliográficos
Autores principales: Hye-Jin Boo, Hye-Young Min, Hyun-Ji Jang, Hye Jeong Yun, John Kendal Smith, Quanri Jin, Hyo-Jong Lee, Diane Liu, Hee-Seok Kweon, Carmen Behrens, J. Jack Lee, Ignacio I. Wistuba, Euni Lee, Waun Ki Hong, Ho-Young Lee
Formato: article
Lenguaje:EN
Publicado: Nature Portfolio 2016
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Acceso en línea:https://doaj.org/article/b677a8e4f78945a8ba09e04a707207e1
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Sumario:The binding of tobacco-specific carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) to nicotinic acetylcholine receptors (nAChRs) induces calcium signalling. Here the authors show that NKK-induced calcium influx in airway epithelial cells triggers IGF2 secretion and tumourigenesis.