Phosphorylated extracellular signal-regulated kinase up-regulated p53 expression in shikonin-induced HeLa cell apoptosis / 中华医学杂志(英文版)
Chinese Medical Journal
;
(24): 671-677, 2005.
Artículo
en Inglés
| WPRIM
| ID: wpr-250864
ABSTRACT
<p><b>BACKGROUND</b>The role of extracellular signal-regulated kinase 1/2 (ERK1/2) in shikonin-induced HeLa cells apoptosis remains vague. This study was to investigate the activation of caspase pathways and the role of ERK1/2 in human cervical cancer cells, HeLa, by shikonin.</p><p><b>METHODS</b>The inhibitory effect of shikonin on the growth of HeLa cells was measured by MTT assay. Fluorescent microscopic analysis of apoptotic cells stained with 4',6'-oliiamiclino-2-phenylindole C (DAPI) and Hoechst 33258 was carried out. Caspase-3 and -8 activities were detected using caspase-3 substrate and caspase-8 substrate as substrates, respectively. The protein levels of ERK, p53 and p-ERK were determined by Western blot analysis.</p><p><b>RESULTS</b>Shikonin inhibited cell growth in a time- and dose-dependent manner. Caspase-3 and caspase-8 were activated in the apoptotic process and caspase inhibitors effectively reversed shikonin-induced apoptosis. Phosphorylation of ERK resulted in up-regulation of p53 expression, which was blocked by mitogen-activated protein kinase (MEK), inhibitor PD 98059.</p><p><b>CONCLUSION</b>Shikonin induces HeLa cell apoptosis through the ERK, p53 and caspase pathways.</p>
Texto completo:
Disponible
Índice:
WPRIM (Pacífico Occidental)
Asunto principal:
Farmacología
/
Fosforilación
/
Fisiología
/
Flavonoides
/
Daño del ADN
/
Células HeLa
/
Regulación hacia Arriba
/
Proteína p53 Supresora de Tumor
/
Naftoquinonas
/
Apoptosis
Límite:
Humanos
Idioma:
Inglés
Revista:
Chinese Medical Journal
Año:
2005
Tipo del documento:
Artículo
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