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目的 观察生长抑素 (Somatostatin ,SST)对Bel74 0 2肝癌细胞株以及裸鼠种植瘤生长的影响 ,同时探索SST的抑瘤机制。方法 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MTT法测量SST对Bel74 0 2细胞增殖的影响 ,光镜下观察细胞形态的变化。以细胞迁移实验和粘附实验观察细胞侵袭和粘附能力的影响。以流式细胞仪测量细胞周期及细胞表面肝细胞生长因子受体Cmet表达的影响 ,以及检测细胞表面生长抑素受体 2 (somatostatinreceptor 2 ,SSTR2 )的阳性率。 结果 SST治疗可以明显抑制裸鼠人肝癌种植瘤的生长 ,但SST处理的 74 0 2细胞增殖能力和细胞形态无明显改变 ,细胞的侵袭和粘附能力可见明显下降 ,细胞生长静止期 (G0 /G1)的比例显著增加 (0 .4 80± 0 .0 32vs 0 .5 77± 0 .0 0 9) ,但未见凋亡峰 ,细胞表面可见SSTR2的表达 ,SST可使细胞Cmet的表达明显受抑。结论 SST能通过与SSTR结合抑制肝癌的生长 ,减少Cmet的表达可能是抑瘤的一个重要机制 ,而并非直接杀死肝癌细胞和诱导凋亡。
Objective To observe the effect of somatostatin (SST) on the growth of Bel74 0 2 hepatocellular carcinoma cell and the implanted tumor in nude mice, and to explore the mechanism of inhibiting tumor growth by SST. Methods The metastatic model of human hepatocellular carcinoma in nude mice was used as material to observe the effect of SST on the growth of implanted tumor. The effect of SST on the proliferation of Bel74 0 2 cells was measured by MTT assay. The morphological changes of cells were observed under light microscope. Cell migration and adhesion experiments were used to observe the effects of cell invasion and adhesion. The cell cycle and the expression of hepatocyte growth factor receptor Cmet on the cell surface were measured by flow cytometry, and the positive rate of somatostatin receptor 2 (SSTR2) on the cell surface was measured. Results SST treatment significantly inhibited the growth of human hepatoma tumor in nude mice. However, the cell proliferation and cell morphology of SST-treated cells did not change significantly. The invasion and adhesion ability of SST cells were significantly decreased. The cell growth arrest (G0 / G1) increased significantly (0.48 ± 0.302 vs. 0.577 ± 0.090), but no apoptotic peak was observed. The expression of SSTR2 was observed on the surface of cells, and the expression of Cmet was significantly increased by SST Suppressed. Conclusion SST can inhibit the growth of hepatocellular carcinoma by binding with SSTR. Reducing the expression of Cmet may be an important mechanism of inhibiting tumor, rather than directly killing the hepatoma cells and inducing apoptosis.