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Cytokine effects on cell survival and death of A549 lung carcinoma cells
dc.creator | Kastamoulas, M. | en |
dc.creator | Chondrogiannis, G. | en |
dc.creator | Kanavaros, P. | en |
dc.creator | Vartholomatos, G. | en |
dc.creator | Bai, M. | en |
dc.creator | Briasoulis, E. | en |
dc.creator | Arvanitis, D. | en |
dc.creator | Galani, V. | en |
dc.date.accessioned | 2015-11-23T10:34:00Z | |
dc.date.available | 2015-11-23T10:34:00Z | |
dc.date.issued | 2013 | |
dc.identifier | 10.1016/j.cyto.2013.01.017 | |
dc.identifier.issn | 1043-4666 | |
dc.identifier.uri | http://hdl.handle.net/11615/29203 | |
dc.description.abstract | Purpose: IL-13, TNF-alpha and IL-1 beta have various effects on lung cancer growth and death, but the signaling pathways mediating these effects have not been extensively analyzed. Therefore, the effects of IL-13, TNF-alpha and IL-1 beta alone, and in combination with Fas, on cell viability and death as well as major signaling pathways involved in these effects were investigated in A549 lung carcinoma cells. Results: Using MU and flow cytometry, IL-13, TNF-alpha and IL-1 beta pretreatment decreased Fas-induced cell death. These anti-cell death effects were attenuated by pretreatment with inhibitors of Nuclear factor-kappa B [NF-kappa B], Phoshatidylinositole-3 kinase [PI3-K], JNK, p38 and ERK1/2 pathways. Results: Using Western blot, IL-13, TNF-alpha and IL-1 beta treated cells showed time-dependent expression of p-ERK1/2, p-p38, p-JNK, p-Akt and p-I kappa B alpha proteins, decreased I kappa B alpha protein expression, no cleavage of Caspase-3 and PARP1 proteins and no notable alterations of Fas protein. IL-13 and TNF-alpha treated cells showed time-dependent increase of FLIPL expression. Conclusion: IL-13, TNF-alpha and IL-1 beta attenuate the pro-cell death effects of Fas on A549 cells, at least partially, by pathways involving the NF-kappa B, PI3-K and MAP kinases, but not by alterations of Fas protein expression. The IL-13 and TNF-alpha cell survival effects may also be due to increased expression of FLIPL protein. (C) 2013 Elsevier Ltd. All rights reserved. | en |
dc.source.uri | <Go to ISI>://WOS:000316577900022 | |
dc.subject | Cytokines | en |
dc.subject | Apoptosis | en |
dc.subject | Lung carcinoma | en |
dc.subject | NF-KAPPA-B | en |
dc.subject | ACTIVATED PROTEIN-KINASE | en |
dc.subject | AIRWAY EPITHELIAL-CELLS | en |
dc.subject | FAS-INDUCED APOPTOSIS | en |
dc.subject | JUN NH2-TERMINAL KINASE | en |
dc.subject | FACTOR-ALPHA | en |
dc.subject | SIGNALING | en |
dc.subject | PATHWAYS | en |
dc.subject | ICAM-1 EXPRESSION | en |
dc.subject | MEDIATED APOPTOSIS | en |
dc.subject | ANTITUMOR IMMUNITY | en |
dc.subject | Biochemistry & Molecular Biology | en |
dc.subject | Cell Biology | en |
dc.subject | Immunology | en |
dc.title | Cytokine effects on cell survival and death of A549 lung carcinoma cells | en |
dc.type | journalArticle | en |
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