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Cobalt chloride stimulates phosphoinositide 3-kinase/Akt signaling through the epidermal growth factor receptor in oral squamous cell carcinoma
Ryu, Mi Heon; Park, Jeong Hee; Park, Ji Eun; Chung, Jin; Lee, Chang Hun; Park, Hae Ryoun.
  • Ryu, Mi Heon; Pusan National University. School of Dentistry. Department of Oral Pathology. Yangsan. KR
  • Park, Jeong Hee; Pusan National University. School of Dentistry. Department of Oral Pathology. Yangsan. KR
  • Park, Ji Eun; Pusan National University. School of Dentistry. Department of Oral Pathology. Yangsan. KR
  • Chung, Jin; Pusan National University. School of Dentistry. Department of Oral Microbiology. Yangsan. KR
  • Lee, Chang Hun; Pusan National University. School of Dentistry. Department of Pathology. Yangsan. KR
  • Park, Hae Ryoun; Pusan National University. School of Dentistry. Department of Oral Pathology. Yangsan. KR
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.
Asunto(s)
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: C‚lulas Año: 2010 Tipo del documento: Artículo País de afiliación: Corea del Sur Institución/País de afiliación: Pusan National University/KR

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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: C‚lulas Año: 2010 Tipo del documento: Artículo País de afiliación: Corea del Sur Institución/País de afiliación: Pusan National University/KR