The p16INK4A Expression in Stomach Cancer , Colon Cancer and Hepatoma Cell Lines.
- Author:
Sun Ju CHOI
1
;
Soo Kie KIM
;
Se Jong KIM
;
Choon Myung KOH
;
Yoon Sun PARK
Author Information
1. Department of Microbiology, Wonju College of Medicine, Yonsei University.
- Publication Type:Original Article
- Keywords:
Cancer cell line;
p16 (INK4A) homozygous deletion;
p16(INK4A) expression
- MeSH:
Blotting, Western;
Carcinogenesis;
Carcinoma, Hepatocellular*;
Cell Cycle;
Cell Line*;
Colon*;
Colonic Neoplasms*;
Cyclin-Dependent Kinase Inhibitor p16;
Gene Deletion;
Gene Silencing;
Genes, Tumor Suppressor;
Humans;
Polymerase Chain Reaction;
Stomach Neoplasms*;
Stomach*
- From:Journal of the Korean Cancer Association
1998;30(3):527-535
- CountryRepublic of Korea
- Language:Korean
-
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.
