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目的研究Hedgehog(Hh)信号通路对环氧合酶2抑制剂塞来昔布介导抗结肠癌效应的影响。方法以胰腺癌PANC-1细胞为对照,采用MTT检测环巴胺20μmol/L和塞来昔布80μmol/L处理后的结肠癌HT-29、LoVo和HCT-116细胞存活率,ELISA法检测胞内胶质瘤相关癌基因同源物1(GLI1)的含量变化。结果环巴胺、塞来昔布均能抑制PANC-1细胞生长和GLI1的含量(P<0.05或P<0.01)。环巴胺处理结肠癌细胞后发现,HT-29和LoVo细胞存活率、GLI1含量降低(P<0.05或P<0.01);其中,LoVo细胞的抑制作用更为显著,而HCT-116细胞生长、GLI1含量无明显变化(P>0.05)。塞来昔布处理结肠癌细胞后发现,HT-29和HCT-116细胞存活率、GLI1含量降低(P<0.05或P<0.01);其中,HCT-116细胞的抑制作用更为显著,而LoVo细胞生长、GLI1含量无明显变化(P>0.05)。结论 Hh信号在LoVo和HT-29细胞是有活性的,而且该信号对LoVo细胞恶性行为维持是必须的。塞来昔布抗结肠癌细胞的作用是有选择性的,可能是通过SMO非依赖的途径来发挥抗癌作用。
Objective To investigate the effect of Hedgehog (Hh) signaling pathway on the anti-colon cancer effect mediated by cyclooxygenase 2 inhibitor celecoxib. Methods Pancreatic cancer PANC-1 cells were used as a control. The survival rates of HT-29, LoVo and HCT-116 colon cancer cells treated with cyclopamine 20μmol / L and celecoxib 80μmol / L were detected by MTT. Changes in the content of glioma related oncogene homolog 1 (GLI1). Results Both cyclopamine and celecoxib inhibited the growth of PANC-1 cells and the content of GLI1 (P <0.05 or P <0.01). After treated with cyclopamine, the survival rates of HT-29 and LoVo cells and GLI1 decreased (P <0.05 or P <0.01), and the inhibitory effect of LoVo cells was more obvious. However, the growth of HCT-116 cells, There was no significant change in GLI1 content (P> 0.05). After treated with celecoxib, the survival rate of HT-29 and HCT-116 cells and the GLI1 content were decreased (P <0.05 or P <0.01). The inhibitory effect of HCT-116 cells was more significant than that of LoVo Cell growth, GLI1 content had no significant change (P> 0.05). Conclusion Hh signaling is active in LoVo and HT-29 cells, and this signal is necessary for the maintenance of malignant behavior in LoVo cells. The effect of celecoxib against colon cancer cells is selective and may exert anti-cancer effects through SMO-independent pathways.