1Department of Microbiology, Wonju College of Medicine, Yonsei University. 2Department of Microbiology, College of Medicine, Yonsei University. 3Institute of Basic Medical Sciences, Wonju College of Medicine, Yonsei University. 4Department of Microbiology, College of Medicine, Kwandong University.
ABSTRACT
PURPOSE: The p16(INK4A) gene encodes a specific inhibitor of cell cycle progression. In recent years, genetic deletion and altered expression of p16(INK4A) gene were frequently showed in many human cancers. So, the p16(INK4A) gene is considered as tumor suppressor gene. However, there has been a few data for the p16(INK4A) in gastric cancer, colon cancer, and hepatoma.So.we investigated the genetic deldtion and altered expression of p16(INK4A) in gastric cancer, colon cancer and hepatoma cell lines.
MATERIALS AND METHODS: The homozygous deletion of p16(INK4A) was examined by using PCR and the protein expression of p16(INK4A) by using Western blotting in cancer cell lines established from Korean patients: stomach cancer, colon cancer and hepatoma cell lines.
RESULTS: Homozygous deletion of p16(INK4A) was detected only 1 stomach cancer cell line out of 13 cell lines examined.
The p16(INK4A) was detected in 3 of 13 cancer cell line.
These results showed the low frequency of p16(INK4A) homozygous deletion and high frequency of p16(INK4A) expression alteration in stomach cancer, colon cancer and hepatoma cell lines.
CONCLUSION: In this study, it may be suggested that the altered pl6(INK4A) expression as well as p16(INK4A) gene deletion play important role in oncogenesis. Further studies to determine the mechanism of p16(INK4A) gene inactivation are expected.
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