Ad-IRF-1 induces apoptosis in esophageal adenocarcinoma.
In: Neoplasia (New York, N.Y.), Jg. 8 (2006), Heft 1, S. 31-7
Online
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Zugriff:
The nuclear transcription factor interferon regulatory factor-1 (IRF-1) is a putative tumor suppressor, but the expression and function of IRF-1 in esophageal adenocarcinoma (EA) remain unknown. We hypothesized that IRF-1 expression was reduced or lost in EA and that restoration of IRF-1 would result in the apoptosis of EA cells in vitro and the inhibition of tumor growth in vivo. Three EA cell lines were used to examine IRF-1 expression, IFN-gamma responsiveness, and the effects of IRF-1 overexpression using a recombinant adenoviral vector (Ad-IRF-1). All three EA cell lines produced IRF-1 protein following IFN-gamma stimulation, although IFN-gamma did not induce cell death. In contrast, Ad-IRF-1 infection resulted in high levels of IRF-1 protein and triggered apoptosis in all three EA cell lines. Potential mechanisms for the differential response to IFN-gamma versus Ad-IRF-1--such as modulation of c-Met or extracellular regulated kinase signaling, or altered expression of IRF-2, Fas, or survivin--were investigated, but none of these mechanisms can account for this observation. In vivo administration of IRF-1 in a murine model of EA modestly inhibited tumor growth, but did not lead to tumor regression. Strategies aimed at increasing or restoring IRF-1 expression may have therapeutic benefits in EA.
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Ad-IRF-1 induces apoptosis in esophageal adenocarcinoma.
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Autor/in / Beteiligte Person: | Watson, GA ; Queiroz de Oliveira, PE ; Stang, MT ; Armstrong, MJ ; Gooding, WE ; Kuan, SF ; Yim, JH ; Hughes, SJ |
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Zeitschrift: | Neoplasia (New York, N.Y.), Jg. 8 (2006), Heft 1, S. 31-7 |
Veröffentlichung: | 2014- : [Amsterdam] : Elsevier ; <i>Original Publication</i>: New York, NY : Stockton Press, c1999-, 2006 |
Medientyp: | academicJournal |
ISSN: | 1476-5586 (electronic) |
DOI: | 10.1593/neo.05559 |
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