Roles of Dopamine in Proliferation of Gastric-Cancer Cells.
10.5230/jkgca.2006.6.3.132
- Author:
Hee Jun JEONG
1
;
Hyun Dong CHAE
Author Information
1. Department of Surgery, Catholic University of Daegu School of Medicine, Daegu, Korea. saxochea@hanmail.net
- Publication Type:Original Article
- Keywords:
Dopamine;
Gastric cancer;
Gastric-cancer cell line;
Dopamine receptors
- MeSH:
Cell Line;
Cell Proliferation;
Cell Survival;
Citrus sinensis;
Dopamine*;
Epithelial Cells;
Ethidium;
Humans;
Neurotransmitter Agents;
Raclopride;
Receptors, Dopamine;
Stomach Neoplasms
- From:Journal of the Korean Gastric Cancer Association
2006;6(3):132-138
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: Dopamine is a neurotransmitter, but in the GIT, the roles of dopamine are a regulator of epithelial cell proliferation, an endogenous protective factor, and a regulator of stomach cancer cell proliferation. By using two different gastric-cancer cell lines, we assessed the effects of dopamine and dopamine receptors on the proliferation of human gastric-cancer cells. MATERIALS AND METHODS: To assess the effects of dopamine and dopamine receptors on the proliferation of human gastric-cancer cells, we investigated cell proliferation and the expression of D1, D2L, and D2S receptor in two gastric-cancer cell lines, SNU 601 and KCU-C2. The effects of dopamine and dopamine receptors on the level of the cell proliferation were determined by staining with an A/H/E (acridine orange, hoechst and ethidium bromide) mixture. RESULTS: After dopamine treatment, the cell viability was significantly decreased in SNU 601 cells (P<0.05) where the D2L receptor was absent, but not in KCU-C2 cells. After treatment with raclopride, a D2 receptor antagonist, dopamine-dose-dependent inhibition of cell proliferation was observed in SNU 601 cells (P<0.05). After treatment with SCH 23390, a D1 receptor antagonist, dopamine significantly increased cell proliferation in KCU-C2 cells (P<0.05), but inhibited cell proliferation in SNU 601 cells (no D2L receptor). CONCLUSION: The dopamine signal via the D1 or the D2S receptor inhibited proliferation of gastric-cancer cells, but that via the D2L receptor increased proliferation. These results suggest that the regulatory effects of dopamine in the gastric-cancer cell proliferation may be controlled by using dopamine receptors.
