【摘要】 目的　观察生长抑素 (SST)对Bel740 2肝癌细胞株增殖侵袭黏附能力和对裸鼠种植瘤生长的影响 ,并对SST抑瘤机制进行一定的探索。方法　以噻唑蓝 (MTT )法测量SST对Bel740 2细胞增殖的影响 ,光镜下观察细胞形态的变化。以细胞迁移实验和黏附实验观察细胞侵袭和黏附能力的影响。以流式细胞仪检测细胞表面肝细胞生长因子受体Cmet和生长抑素受体 2(SSTR2 )的表达和细胞周期的影响。以裸鼠人肝癌转移模型为材料 ,观察SST对种植瘤生长的影响 ,以免疫组织化学观察SSTR2和Cmet的表达影响。结果　SST处理的 740 2细胞增殖能力和细胞形态无明显改变 ,细胞的侵袭和黏附能力明显下降 ,细胞生长静止期 (G0 /G1)的比例显著增加 ,但未见凋亡峰 ,细胞表面Cmet的表达明显受抑 ,但SSTR2的表达增加 ,裸鼠人肝癌种植瘤在SST治疗后生长受到明显抑制 ,免疫组织化学也可见种植瘤内SSTR2表达增加 ,而Cmet的表达明显受抑制。结论　SST通过与SSTR起作用抑制肝癌的生长 ,减少Cmet的表达是SST起作用的重要方式。此外 ,长期的SST治疗可以上调SSTR2的表达 ,加大SST抑制肝癌的效果 ,但短期的处理反而诱导SSTR2的脱敏和抑瘤效果下降。更多还原

【Abstract】 Objective To observe the inhibitiory effects and mechanism of Somatostatin (SST) on the growth of Bel7402 hepatocellular carcinoma (HCC) cell line and HCC xenografts in nude mice.Methods The effect of SST on proliferative ability of Bel7402 cells was observed by methabenzthiazuron (MTT) assay and the changes in cell morphology under light microscopy.The adhesive and invasive ability of 7402 cells was measured via cell adhesion and migration experiments.The cell cycle,the Cmet (hepatocyte growth factor repceptor) and SST receptor 2 (SSTR2) expression of 7402 cells were detected by immunofluorescence flow cytometry.Nude mice bearing xenografts of cell line were treated with SST or saline (control group) for 7 weeks until tumor implantation.The immunohistochemistry for SSTR2 and Cmet was performed.Results After the treatment withSST,the proliferative ability and cell morphology of 7402 cells didn’t change signiFicantly.The adhesive and invasive ability was decreased significantly.The ratio of cells in resting state (G0/G1) was increased,but no apoptosis peak was observed.The Cmet and SSTR2 expression on 7402 cells membranes was decreased significantly.The mean tumor weight in mice treated with SST was significantly less than that of the control group.In immunohistochemistry,SSTR2 immunostaining in tumor cells of treatment group showed stronger positivity than that of control group.Conveersely,the intensity of Cemt immunolabeling was decresed obviously after the treatment.Conclusion SST could inhibit the growth of HCC through combining with SSTR.The long-term SST treatment can increase the SSTR2 expression and enlarge the effect of inhibiting HCC though short-term treatment may induces its desensitization.The decrease of the Cmet expression in HCC cells may play an important role in SST inhibiting HCC.更多还原