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KMID : 0829220090330020069
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Korean Journal of Oral and Maxillofacial Pathology
2009 Volume.33 No. 2 p.69 ~ p.74
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Cobalt Chloride, a Chemical Hypoxic Agent, Activates Erk Kinase Through the Epidermal Growth Factor Receptor in Oral Squamous Cell Carcinoma Cells
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Park Jeong Hee
Park Hae-Ryoun
Park Bong-Soo
Park Ji-Eun
Chung Jin
Ryu Mi-Heon
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Abstract
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Tumor cells under hypoxic conditions are often found due to the rapid outgrowth of their vascular supply, and,in order to survive hypoxia, these cells induce numerous signaling factors. Erk is an important kinase in cell survival, and its activity is regulated by Raf kinases through numerous growth factor receptors. The authors investigated Erk activation and Raf/Erk signaling using the hypoxia-mimetic agent, cobalt chloride (CoCl2), in oral squamous cell carcinoma (OSCC) cells. CoCl2 increases Erk phosphorylation in both a dose- and time-dependent manner. In addition, blocking the activation of epidermal growth factor receptor (EGFR) using PD168393 abolished Erk activation in response to CoCl2, suggesting that Erk phosphorylation by CoCl2 is dependent on EGFR.
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KEYWORD
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Hypoxia, Cobalt chloride, PI3K/Akt, PDK1, PTEN, EGFR, Erk, Raf-1, Oral squamous cell carcinoma
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