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Over-expression of hypoxia-inducible factor-1 alpha increases angiogenesis of LNCaP cells / 中华男科学杂志
National Journal of Andrology ; (12): 988-991, 2007.
Artículo en Chino | WPRIM | ID: wpr-232026
ABSTRACT
<p><b>OBJECTIVE</b>To evaluate the effect of hypoxia-inducible factor-1 alpha (HIF-la) on angiogenesis in human prostate cancer cells.</p><p><b>METHODS</b>Human prostate cancer cells of the line LNCaP were cultured and transfected by the recombinant plasmid pcDNA3. 1(-)/HIF-1alpha containing the gene HIF-1alpha with the Lipofectamine 2000 system. The positive clone cells were selected by G418 and confirmed by Western blotting and immunofluorescence (LNCaP/HIF-1alpha cells). The expressions of VEGF, iNOS and Ang-2 were detected by Western blotting.</p><p><b>RESULTS</b>The expression of HIF-1alpha in the LNCaP/HIF-1alpha cells was distinctly higher than that in the LN-CaP cells. Compared with the LNCaP cells, the expressions of VEGF and iNOS were up-regulated, whereas Ang-2 remained unchanged in the LNCaP/HIF-1alpha cells.</p><p><b>CONCLUSION</b>The over-expression of HIF-1alpha can induce an increase in angiogenesis proteins and improve the angiogenesis potency of prostate cancer.</p>
Asunto(s)
Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Patología / Plásmidos / Neoplasias de la Próstata / Transfección / Química / Western Blotting / Técnica del Anticuerpo Fluorescente / Óxido Nítrico Sintasa / Línea Celular Tumoral / Factor A de Crecimiento Endotelial Vascular Límite: Humanos / Masculino Idioma: Chino Revista: National Journal of Andrology Año: 2007 Tipo del documento: Artículo

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Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Patología / Plásmidos / Neoplasias de la Próstata / Transfección / Química / Western Blotting / Técnica del Anticuerpo Fluorescente / Óxido Nítrico Sintasa / Línea Celular Tumoral / Factor A de Crecimiento Endotelial Vascular Límite: Humanos / Masculino Idioma: Chino Revista: National Journal of Andrology Año: 2007 Tipo del documento: Artículo