scholarly journals Beauvericin-induced cell apoptosis through the mitogen-activated protein kinase pathway in human nonsmall cell lung cancer A549 cells

2016 ◽  
Vol 41 (3) ◽  
pp. 429-437 ◽  
Author(s):  
Chien-Lin Lu ◽  
Hen-I Lin ◽  
Bing-Fang Chen ◽  
Guey-Mei Jow
Keyword(s):  
Lung Cancer ◽  
Protein Kinase ◽  
Cell Lung Cancer ◽  
Cell Apoptosis ◽  
A549 Cells ◽  
Nonsmall Cell Lung Cancer ◽  
Mitogen Activated Protein Kinase ◽  
Mitogen Activated Protein ◽  
Kinase Pathway

scholarly journals Oxytocin- and vasopressin-induced growth of human small-cell lung cancer is mediated by the mitogen-activated protein kinase pathway

2004 ◽  
Vol 11 (4) ◽  
pp. 871-885 ◽  
Author(s):  
C Péqueux ◽  
B P Keegan ◽  
M-T Hagelstein ◽  
V Geenen ◽  
J-J Legros ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Protein Kinase ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Mitogen Activated Protein Kinase ◽  
Thymidine Uptake ◽  
Small Cell Lung ◽  
Cell Lung Carcinoma ◽  
Mitogen Activated Protein

Malignant growth of small-cell lung carcinoma is promoted by various neuroendocrine autocrine/paracrine loops. Therefore, to interfere with this mitogenic process, it is crucial to elucidate the mechanisms involved. It is known that the oxytocin (OT) and vasopressin (VP) genes, normally transcriptionally restricted in their expression, are activated in small-cell lung cancer (SCLC), concomitantly with expression of their receptors (OTR, V1aR, V1bR/V3R and V2R). The aim of the present study was to characterize, in concentrations close to physiological and pharmacological conditions, intracellular signalling events triggered by OT and VP binding to their specific receptors in SCLC cells and to identify factors mediating OT- and VP-induced mitogenic effects on SCLC. Known agonists for OTR ([Thr4,Gly7]OT) and V1aR (F180), in addition to OT and VP, were able to elicit increases in cytosolic Ca2+ levels and this effect could be blocked using an OTR antagonist (OVTA) or a V1aR antagonist (SR49059) respectively. There was no activation of the cAMP pathway detected after VP, dDAVP (a V2R agonist), or OT treatment. Stimulation of SCLC cells with OT and VP led to an increase of extracellular signal-regulated kinase (ERK) 1/2 phosphorylation, maximal at 5 min, and the subsequent phosphorylation of its downstream target p90 ribosomal S6 kinase (p90RSK). Pre-incubation with OVTA and SR49059, and with inhibitors of phospholipase C (PLC), protein kinase C (PKC), mitogen-activated protein kinase/ERK kinase (MEK) 1/2 and a Ca2+ chelator significantly reduced OT- and VP-induced ERK1/2 phosphorylations. OVTA, SR49059 as well as MEK1/2 and PKC inhibitors also downregulated OT- and VP-induced p90RSK phosphorylation. In [3H]thymidine-uptake experiments, we subsequently observed that PLC, Ca2+, PKC and ERK1/2 are absolutely required for the OT- and VP-stimulated SCLC cellular growth process. In conclusion, the results presented here indicate that OT- and VP-induced mitogenic effects on SCLC are respectively mediated by OTR and V1aR signalling and that this mitogenic signalling passes through the phosphorylation of ERK1/2 and p90RSK in a PLC-, Ca2+-, PKC- and MEK1/2-dependent pathway.

scholarly journals Mutations in BRAF and KRAS Converge on Activation of the Mitogen-Activated Protein Kinase Pathway in Lung Cancer Mouse Models

2007 ◽  
Vol 67 (10) ◽  
pp. 4933-4939 ◽  
Author(s):  
Hongbin Ji ◽  
Zhenxiong Wang ◽  
Samanthi A. Perera ◽  
Danan Li ◽  
Mei-Chih Liang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Protein Kinase ◽  
Mouse Models ◽  
Mitogen Activated Protein Kinase ◽  
Mitogen Activated Protein ◽  
Kinase Pathway
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