Cobalt chloride stimulates phosphoinositide 3-kinase/Akt signaling through the epidermal growth factor receptor in oral squamous cell carcinoma
Biocell
;
34(1): 15-21, Apr. 2010. graf
Artículo
en Inglés
| LILACS
| ID: lil-595046
ABSTRACT
Tumor cells are often found under hypoxic conditions due to the rapid outgrowth of their vascular supply, and, in order to survive hypoxia, these cells induce numerous signaling factors. Akt is an important kinase in cell survival, and its activity is regulated by the upstream phosphoinositide 3-kinase (PI3K) and receptor tyrosine kinases (RTKs). In this study, we examined Akt activation and RTKs/PI3K/Akt signaling using the hypoxia-mimetic cobalt chloride in oral squamous carcinoma cells. Cobalt chloride increases Akt phosphorylation in both a dose- and time-dependent manner. Blocking the activation of the PI3K/Akt pathway using LY294002 abolished Akt activation in response to cobalt chloride, suggesting that Akt phosphorylation by cobalt chloride is dependent on PI3K. In addition, activation of the PI3K/Akt path way seems to rely on the epidermal growth factor receptor (EGFR), since the inhibition of EGFR attenuated cobalt chloride-induced Akt activation. The results in this study also demonstrate that cobalt chloride increases EGFR protein levels and induces oral squamous cell carcinoma cells to enter S phase.
Texto completo:
Disponible
Índice:
LILACS (Américas)
Asunto principal:
ADN de Neoplasias
/
Neoplasias de la Boca
/
Carcinoma de Células Escamosas
/
Hipoxia de la Célula
/
Cobalto
/
Proteínas Proto-Oncogénicas c-akt
Límite:
Humanos
Idioma:
Inglés
Revista:
Biocell
Asunto de la revista:
Clulas
Año:
2010
Tipo del documento:
Artículo
País de afiliación:
Corea del Sur
Institución/País de afiliación:
Pusan National University/KR
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