Camptothecin-nduced Apoptosis in Gastric Cancer Cell Lines: Involvement of Bcl-.
- Author:
Yoon Jeung CHA
1
;
Young Don MIN
;
Cheol Hee CHOI
Author Information
1. Departments of General Surgery, Chosun University Medical College, Kwangju, Korea.
- Publication Type:Original Article
- Keywords:
Apoptosis;
Gastric cancer;
Bcl-
- MeSH:
Antineoplastic Agents;
Apoptosis*;
Biological Therapy;
Blotting, Western;
Camptothecin;
Cell Death;
Cell Line*;
DNA;
DNA Fragmentation;
DNA Topoisomerases, Type I;
Drug Therapy;
Electrophoresis, Agar Gel;
Microscopy, Electron;
Stomach Neoplasms*
- From:Journal of the Korean Surgical Society
1998;55(6):800-808
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Apoptosis can be induced by various anticancer agents. Resistance to apoptosis may play an important role in tumors refractory to chemotherapy. The authors investigated both the induction of apoptosis by camptothecin, a topoisomerase I inhibitor, in gastric cancer cell lines and the roles of apoptosis-elated gene products. METHODS: Two gastric cancer cell lines, SNU- and SNU-6, were examined for response to chemotherapeutic agents. Cytotoxicity was determined by a MTT assay. Apoptosis was measured by a DNA fragmentation assay using agarose gel electrophoresis and electron microscopy. Apoptosis-elated gene products were determined by western blot analysis. RESULTS: The two gastric cancer cell lines (SNU- and SNU-6) showed different sensitivities to camptothecin. Apoptosis of SNU-6 was easily induced by camptothecin, while SNU- was refractory to apoptosis, which was confirmed by DNA fragment assays and electron microscopy. Western blot analysis revealed that the amount of Bcl- in SNU- was 2.68-imes more than that in SNU-6. There were no differences in the levels of Bax, Bcl-L, Bcl-s, and p53 between the two cell lines. CONCLUSIONS: It is thought that Bcl- may play an important role in blocking cell death due to anticancer drugs in gastric cancer cell lines. Thus, chemosensitivity might be increased if this cell death-locking status were to be modified by new biologic therapies for gastric cancer.
