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Original Article
- Modulation of Telomerase Activity by p53 Gene in KATO - III Gastric Carcinoma Cell Line
- Si Young Kim, Kyung Sam Cho, Jae Kyung Park, Young II Kim, Hwi Joong Yoon
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Journal of the Korean Cancer Association 1999;31(6): 1112-1119.
1Department of Internal Medicine, School of Medicine, Kyung Hee University, Seoul, Korea.
2Division of Medical Science Study, East-West Medical Research Institute, Kyung Hee University, Seoul, Korea.
2Division of Medical Science Study, East-West Medical Research Institute, Kyung Hee University, Seoul, Korea.
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Abstract
PURPOSE
Alteration of p53 and telomerase activity may be responsible for gastric carcino- genesis. In this study, we tried to observe modulation of telomerase activity by wild type p53 in gastric cancer cell lines.
MATERIALS AND METHODS
We used five gastric cancer cell lines (KATO-III, AGS, SNU-1, SNU-5, SNU-16). In order to find p53 mutation, we used western blot and PCR-SSCP. The TRAP-eze kit which supplied by Oncor (Gaithersburg, MD) was used to detect telomerase activity of the five gastric carcinoma cell lines. The wild type p53 gene was transfected by electroporation method.
RESULTS
The expression of p53 protein was increased in four gastric carcinoma cell lines and one cell line (KATO-III) did not express. We found p53 point mutation in exon 5 and 8, and the p53 gene was deleted in KATO-III. The telomerase activity were observed in all five gastric carcinoma cell lines and there were no difference in telomere repeat length among five cell lines. After transfection with wild type p53, we could not find the change of telomerase activity in KATO-III.
CONCLUSION
Although activation of telomerase activity and mutation of p53 gene may be needed in gastric carcinogenesis, the telomerase activity was not affected by restoration of p53 function in gastric carcinoma cell lines.
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