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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。
Objective To observe the effect of somatostatin (SST) on the proliferation, invasion and adhesion of Bel740 2 hepatocarcinoma cell line and the growth of implanted tumor in nude mice, and to explore the mechanism of tumor suppressor gene SST. Methods The effect of SST on the proliferation of Bel740 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 effect of cell invasion and adhesion. The effects of Cmet and somatostatin receptor 2 (SSTR2) on cell surface and cell cycle were detected by flow cytometry. The metastasis 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 expression of SSTR2 and Cmet was observed by immunohistochemistry. Results The proliferation and cell morphology of 7402 cells treated with SST had no significant changes, the cell invasion and adhesion decreased significantly, and the proportion of G0 / G1 increased significantly, but no apoptotic peak was observed. The cell surface Cmet However, the expression of SSTR2 was increased. The growth of human hepatocellular carcinoma in nude mice was significantly inhibited after SST treatment. The expression of SSTR2 in the tumor was also observed by immunohistochemistry, while the expression of Cmet was significantly inhibited. Conclusion SST can inhibit the growth of hepatocellular carcinoma through its interaction with SSTR, and reducing the expression of Cmet is an important way of SST. In addition, long-term treatment with SST can up-regulate the expression of SSTR2 and increase the inhibitory effect of SST on hepatocellular carcinoma. However, short-term treatment can induce desensitization and anti-tumor effect of SSTR2.