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.

I. INTRODUCTION
 II. MATERIALS AND METHODS
  1. Cell culture
  2. Reagents
  3. Western blot analysis
 III. RESULTS
  1. Identification of an Akt activator in OSCC cellsunder hypoxic condition induced by CoCl2
  2. CoCl2 activates Erk in a Raf kinase-independentmechanism
  3. Erk activation by CoCl2 treatment occurs throughEGFR
  4. Activities of PTEN and PDK1 is independent onEGFR signaling
 IV. DISCUSSION
 V. REFERENCES

• 박정희(Department of Oral Pathology) | Jeong Hee Park1
• 박지은(Department of Oral Pathology) | Ji Eun Park
• 정진(Department of Oral Microbiology) | Jin Chung
• 박봉수(Department of Oral Anatomy) | Bong Soo Park
• 유미현(Department of Oral Pathology) | Mi Heon Ryu
• 박혜련(Department of Oral Pathology) | Hae Ryoun Park correspondence