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Regulation of Cisplatin Resistance in Lung Cancer Cells by Nicotine, BDNF, and a ß-Adrenergic Receptor Blocker.
Ray, Ravel; Al Khashali, Hind; Haddad, Ben; Wareham, Jadziah; Coleman, Kai-Ling; Alomari, Danyah; Ranzenberger, Robert; Guthrie, Jeffrey; Heyl, Deborah; Evans, Hedeel Guy.
Afiliación
  • Ray R; Chemistry Department, Eastern Michigan University, Ypsilanti, MI 48197, USA.
  • Al Khashali H; Chemistry Department, Eastern Michigan University, Ypsilanti, MI 48197, USA.
  • Haddad B; Chemistry Department, Eastern Michigan University, Ypsilanti, MI 48197, USA.
  • Wareham J; Chemistry Department, Eastern Michigan University, Ypsilanti, MI 48197, USA.
  • Coleman KL; Chemistry Department, Eastern Michigan University, Ypsilanti, MI 48197, USA.
  • Alomari D; Chemistry Department, Eastern Michigan University, Ypsilanti, MI 48197, USA.
  • Ranzenberger R; Chemistry Department, Eastern Michigan University, Ypsilanti, MI 48197, USA.
  • Guthrie J; Chemistry Department, Eastern Michigan University, Ypsilanti, MI 48197, USA.
  • Heyl D; Chemistry Department, Eastern Michigan University, Ypsilanti, MI 48197, USA.
  • Evans HG; Chemistry Department, Eastern Michigan University, Ypsilanti, MI 48197, USA.
Int J Mol Sci ; 23(21)2022 Oct 24.
Article en En | MEDLINE | ID: mdl-36361620
It is well-recognized that cigarette smoking is a primary risk factor in the development of non-small cell lung cancer (NSCLC), known to account for ~80% of all lung cancers with nicotine recognized as the major addictive component. In investigating the effect of nicotine, brain-derived neurotrophic factor (BDNF), and the ß-adrenergic receptor blocker, propranolol, on sensitivity of NSCLC cell lines, A549 and H1299, to cisplatin, we found increased cell viability, and enhanced cisplatin resistance with nicotine and/or BDNF treatment while opposite effects were found upon treatment with propranolol. Cell treatment with epinephrine or nicotine led to EGFR and IGF-1R activation, effects opposite to those found with propranolol. Blocking EGFR and IGF-1R activation increased cell sensitivity to cisplatin in both cell lines. PI3K and AKT activities were upregulated by nicotine or BDNF and downregulated by cell treatment with inhibitors against EGFR and IGF-1R and by propranolol. Apoptosis and cell sensitivity to cisplatin increased upon co-treatment of cells with cisplatin and inhibitors against PI3K or AKT. Our findings shed light on an interplay between nicotine, BDNF, and ß-Adrenergic receptor signaling in regulating survival of lung cancer cells and chemoresistance which can likely expand therapeutic opportunities that target this regulatory network in the future.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Carcinoma de Pulmón de Células no Pequeñas / Neoplasias Pulmonares Tipo de estudio: Risk_factors_studies Límite: Humans Idioma: En Revista: Int J Mol Sci Año: 2022 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Suiza
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Carcinoma de Pulmón de Células no Pequeñas / Neoplasias Pulmonares Tipo de estudio: Risk_factors_studies Límite: Humans Idioma: En Revista: Int J Mol Sci Año: 2022 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Suiza