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Journal of Southern Medical University ; (12): 1152-1160, 2007.
Artículo en Chino | WPRIM | ID: wpr-337308

RESUMEN

<p><b>OBJECTIVE</b>To study the effect of the adenovirus containing CD/TK fusion gene controlled by the human vascular endothelial growth factor (VEGF) promoter on apoptosis of human gastric carcinoma cells SGC-7901.</p><p><b>METHODS</b>VEGF-expressing SGC-7901 cells were infected by the recombinant adenovirus Ad-VEGFP-CD/TK, and the infection efficiencies were observed with fluorescence microscopy. The toxic effect and intracellular calcium concentration induced by 5-fluorocytosine (5-FC) and ganciclovic (GCV) were determined by light microscopy, electron microscopy and flow cytometry.</p><p><b>RESULTS</b>The transfection efficiency of the recombinant adenovirus in SGC-7901 cells increased with the viral titer. At the multiplicity of infection (MOI) of 100, 5-FC and GCV could induce apoptosis of SGC-7901 cells within a given dose range in a dose- and time-dependent manner, and apoptotic changes of the cells were observed with electron microscopy. Apoptotic peak was also detected by flow cytometry. Cell cycle analysis revealed increased cell percentage in G(0)-G(1) phase and decreased percentage of cells in G(2)-M and S phases in response to treatment with the pro-drugs, which also induced marked elevation of intracellular calcium concentration in the infected cells.</p><p><b>CONCLUSIONS</b>CD/TK fusion gene system driven by VECF promoter selectively induces apoptosis of VEGF-expressing SGC-7901 cells, the action of which is probably mediated by intracellular calcium variation.</p>


Asunto(s)
Animales , Humanos , Adenoviridae , Genética , Fisiología , Apoptosis , Genética , Calcio , Metabolismo , Línea Celular Tumoral , ADN , Metabolismo , ADN Recombinante , Genética , Relación Dosis-Respuesta a Droga , Flucitosina , Farmacología , Ganciclovir , Farmacología , Genes Transgénicos Suicidas , Genética , Microscopía Electrónica , Regiones Promotoras Genéticas , Genética , Neoplasias Gástricas , Genética , Metabolismo , Patología , Virología , Factor A de Crecimiento Endotelial Vascular , Genética
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