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目的 研究应用肿瘤坏死因子 (TNF α)单独处理SMMC 772 1肝癌细胞不能引起肝癌细胞凋亡的原因。方法 采用免疫组化ABC法 ,结合图像分析仪及流式细胞术和Western印迹方法测定SMMC 772 1细胞表面E 钙粘蛋白 (E cadherin)、α5β1整合蛋白 (α5β1intergrin)、粘着斑激酶 (FAK )表达及粘着斑激酶磷酸化的程度。结果 在肿瘤坏死因子的作用下 ,E 钙粘蛋白的表达略有下降 ,但无明显差异。整合蛋白α5亚基的表达明显下降 ,而整合蛋白 β1亚基表达基本无变化。粘着斑激酶的蛋白表达随着肿瘤坏死因子浓度的增加略有下降 ,但变化不明显 ,粘着斑激酶的磷酸化程度无明显的变化。结论 单独用肿瘤坏死因子处理SMMC 772 1肝癌细胞后 ,并没有阻断由整合蛋白α5β1亚基及E 钙粘蛋白介导的 2条信号通路 ,且由胱冬肽酶 (caspases)介导的凋亡也没有被完全启动 ,不足以引起细胞的凋亡。
Objective To study the effect of tumor necrosis factor (TNF α) treatment alone on SMMC 772 1 hepatocarcinoma cells not causing apoptosis of hepatoma cells. Methods The expression of E cadherin, α5β1 intergrin, and focal adhesion kinase (FAK) on SMMC 772 1 cells was determined by immunohistochemical ABC method combined with image analyzer, flow cytometry and Western blot. And the extent of focal kinase kinase phosphorylation. Results Under the effect of tumor necrosis factor, the expression of E-cadherin was slightly decreased, but there was no significant difference. The expression of integrin α5 subunit was significantly decreased, while the expression of integrin β1 subunit was almost unchanged. The protein expression of focal adhesion kinase decreased slightly with the increase of tumor necrosis factor concentration, but the change was not obvious. There was no significant change in the phosphorylation of focal adhesion kinase. Conclusions Treatment of SMMC 772 1 liver cancer cells with tumor necrosis factor alone did not block the two signaling pathways mediated by integrin α5β1 subunit and E-cadherin, and was mediated by caspase. The death has not been fully activated and is not sufficient to cause cell apoptosis.