[Effect of a selective COX-2 inhibitor on cell proliferation and apoptosis in human gastric cancer cell line BGC-823].
Qian Li, Jie Peng, Guiying Zhang
Abstract
Qian Li, Jie Peng, Guiying Zhang
Abstract
OBJECTIVE: To determine the effect of a selective COX-2 inhibitor celecoxib on cell proliferation and apoptosis of gastric cancer cell line BGC-823 to seek an effective and safe drug for gastric cancer chemoprevention. METHODS: Gastric cancer cell line BGC-823 was cultured to 80% fusion. MTT assay and flow cytometry were used to quantify the influence of celecoxib in the proliferation, cell period, and apoptosis of gastric cancer cell line BGC-823. The expression of p21 and Fas by RT-PCR were investigated on gastric cancer cell line BGC-823 by the effect of different celecoxib concentrations. RESULTS: Growth of BGC-823 cells was inhibited by celecoxib in a dose-and time-dependent manner (P<0.05).Flow cytometry showed that celecoxib increased the proportion of cells in G1 phase, whereas decreased the proportion of cells in S phase and increased the apoptotic rates of cells in a concentration-dependent manner from 0 to 100 micromol/L in gastric cancer cell line BGC-823 (P<0.05). RT-PCR detection showed that the treated BGC-823 cells had increased the expression of p21 and Fas, which was also in a dose-dependent manner (P<0.05). CONCLUSION: Celecoxib inhibited cell proliferation and apoptosis of human gastric cancer cell line BGC-823, which may be related to blocking the cell cycle progress by increasing the expression of p21 and inducing the apoptosis of gastric cancer cells by increasing the expression of Fas.
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OBJECTIVE: To determine the effect of a selective COX-2 inhibitor celecoxib on cell proliferation and apoptosis of gastric cancer cell line BGC-823 to seek an effective and safe drug for gastric cancer chemoprevention. METHODS: Gastric cancer cell line BGC-823 was cultured to 80% fusion. MTT assay and flow cytometry were used to quantify the influence of celecoxib in the proliferation, cell period, and apoptosis of gastric cancer cell line BGC-823. The expression of p21 and Fas by RT-PCR were investigated on gastric cancer cell line BGC-823 by the effect of different celecoxib concentrations. RESULTS: Growth of BGC-823 cells was inhibited by celecoxib in a dose-and time-dependent manner (P<0.05).Flow cytometry showed that celecoxib increased the proportion of cells in G1 phase, whereas decreased the proportion of cells in S phase and increased the apoptotic rates of cells in a concentration-dependent manner from 0 to 100 micromol/L in gastric cancer cell line BGC-823 (P<0.05). RT-PCR detection showed that the treated BGC-823 cells had increased the expression of p21 and Fas, which was also in a dose-dependent manner (P<0.05). CONCLUSION: Celecoxib inhibited cell proliferation and apoptosis of human gastric cancer cell line BGC-823, which may be related to blocking the cell cycle progress by increasing the expression of p21 and inducing the apoptosis of gastric cancer cells by increasing the expression of Fas.
Key concepts: Apoptosis, Celecoxib, Flow cytometry, Cell cycle, Cell growth, Cell culture, Cancer, Cancer cell