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目的观察非甾体类抗炎药塞来昔布对体外培养的人结肠癌SW480细胞增殖和凋亡的影响,并研究其与Wnt/β-catenin信号通路的关系,探讨塞来昔布抑制结肠肿瘤生长的分子机制。方法应用MTT法测定不同浓度塞来昔布(0、20、40、60、80、100μmol/L)对SW480细胞增殖的影响;应用流式细胞术分析不同浓度塞来昔布(0、20、40、80μmol/L)处理48 h后对SW480细胞凋亡的影响;应用Western blot法分析不同浓度塞来昔布(0、20、40、80μmol/L)处理48 h后SW480细胞中β-catenin蛋白和磷酸化的β-catenin蛋白的表达水平。结果 MTT结果显示,塞来昔布对结肠癌细胞的增殖抑制有浓度依赖性和时间依赖性(P<0.05);流式细胞术分析显示,随着塞来昔布浓度的增加,结肠癌细胞的凋亡率明显增加(P<0.05);Western blot法检测结果显示,随着塞来昔布浓度的增加,β-catenin蛋白表达显著下降(P<0.05),而磷酸化的β-catenin蛋白表达显著升高(P<0.05),且呈剂量依赖性。结论塞来昔布可以抑制结肠癌SW480细胞的Wnt/β-catenin信号通路,这可能是其抑制结肠癌细胞增殖、促进凋亡的重要机制。
Objective To investigate the effect of non-steroidal anti-inflammatory drug celecoxib on the proliferation and apoptosis of human colon carcinoma SW480 cells in vitro and its relationship with the Wnt / β-catenin signaling pathway and to investigate the effect of celecoxib on colon Molecular mechanisms of tumor growth. Methods The effects of different concentrations of celecoxib (0, 20, 40, 60, 80 and 100 μmol / L) on the proliferation of SW480 cells were determined by MTT assay. The effects of different concentrations of celecoxib 40, 80μmol / L) for 48 h, the effects of different concentrations of celecoxib (0, 20, 40 and 80μmol / L) on the apoptosis of SW480 cells were detected by Western blot. Protein and phosphorylated β-catenin protein expression levels. Results MTT results showed that celecoxib inhibited the proliferation of colon cancer cells in a concentration-dependent and time-dependent manner (P <0.05). Flow cytometry analysis showed that with the increase of celecoxib concentration, colon cancer cells (P <0.05). The results of Western blot showed that the expression of β-catenin was significantly decreased with the increase of celecoxib concentration (P <0.05), while the phosphorylated β-catenin protein The expression was significantly increased (P <0.05), and in a dose-dependent manner. Conclusion Celecoxib can inhibit the Wnt / β-catenin signaling pathway in colon cancer SW480 cells, which may be an important mechanism of its inhibition of colon cancer cell proliferation and apoptosis.