Adenovirus-mediated IL-24 confers radiosensitization to human lung adenocarcinoma in vitro and in vivo
The current paper aims to study the effect of adenovirus-mediated IL-24 (Ad-IL-24) on human lung adenocarcinoma in vitro and in vivo and determine its possible mechanism of action. The growth-suppressing and apoptosis-inducing effects of Ad-IL-24, radiotherapy, and Ad-IL-24+ radiotherapy (hereinafte...
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Veröffentlicht in: | Molecular biology reports 2015-06, Vol.42 (6), p.1069-1080 |
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Sprache: | eng |
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Zusammenfassung: | The current paper aims to study the effect of adenovirus-mediated IL-24 (Ad-IL-24) on human lung adenocarcinoma in vitro and in vivo and determine its possible mechanism of action. The growth-suppressing and apoptosis-inducing effects of Ad-IL-24, radiotherapy, and Ad-IL-24+ radiotherapy (hereinafter referred to as the joint group) on SPC-A1 lung carcinoma cells were assessed by using 3-(4,5-dimethyliazolyl-2)-2,5-diphnyltetrazolium bromide and flow cytometry. A human lung model was established with SPC-A1 cells in nude mice. Groups of mice were subjected to multi-point injections to their tumors. Gross tumor volumes were measured dynamically. The ratios of tumor suppression and radiosensitization effect were evaluated according to the method of probability sum Q values. The expressions of Bax, Bcl-2, Survivin, and Caspase-3 in tumor samples were detected by immunohistochemistry. The ratios of inhibition and apoptosis in the joint group were higher than those in the individual Ad-IL-24 and radiotherapy groups. In vitro, the joint group suppressed tumor growth conspicuously, showing a weight inhibition rate of about 64 %. The expressions of FasL, Bax and Caspase-3 were upregulated in the joint group, while the expressions of Cox,Bcl-2,VEGF,CD34 and Survivin were downregulated. The current study proves that Ad-IL-24 suppresses growth of SPC-A1 cells both in vitro and in vivo. Its functions appear to be related to cell apoptosis and antiangiogenesis. |
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ISSN: | 0301-4851 1573-4978 |
DOI: | 10.1007/s11033-014-3846-6 |