中文摘要：

目的研究沉默TCA8113舌癌细胞整合素连接激酶（integrin-linked kinase,ILK）基因的表达,对其下游底物Akt和GSK3β磷酸化状态及对移植瘤生长和自发性转移的影响。方法通过Lipofectamine 2000介导将特异性siILK表达载体和无同源性的对照载体,稳定转染人舌鳞癌TCA8113细胞,分为TCA8113组、TCA8113 vector组和TCA8113 siILK组,将3组细胞分别注入裸鼠皮下构建移植瘤模型,5周后检测瘤质量,对裸鼠肺及瘤组织形态学行常规病理学检查,使用免疫荧光技术检测体外和体内癌细胞p-Akt和p-GSK3β等的表达,并观察瘤组织内血管生成情况。结果 TCA8113组、TCA8113 vector组肺组织均发生自发性转移瘤,TCA8113 siILK组肺组织未发现自发性转移瘤;TCA8113 siILK组移植瘤细胞形态较其他2组体积减小,核分裂象较少,核浆比例缩小;TCA8113 siILK组在体内和体外实验中的p-Akt和p-GSK3β表达较其他2组均明显下降（P〈0.05）;TCA8113 siILK组移植瘤质量较其他2组显著降低（P〈0.05）,抑瘤率分别为84%和92%;TCA8113 siILK组移植瘤血管生成较其他2组也明显减少（P〈0.05）。结论沉默TCA8113舌癌细胞ILK表达可抑制其下游信号传导分子Akt和GSK3β的磷酸化,并抑制移植瘤血管生成,从而抑制移植瘤的生长。

英文摘要：

Objective To determine the effects of silencing integrin-linked kinase （ILK） in human tongue cancer TCA8113 cells on the expression of its downstream signal molecules p-Akt and p-GSK3β and on the growth and spontaneous metastasis of tumor xenografts. Methods Target cells were constructed by transfecting specific siILK plasmid and a non-homologous vector negative control into TCA8113 cells, TCA8113 examination. Changes in the expression of p-Akt, p-GSK313 and micro-blood vessels in tumor tissue were detected by immunofluorescence assay and laser scanning confocal microscopy. Results Spontaneous lung metastasis tumors were found both in TCAS113 and TCASll3 vector group, while there was no such finding in the lungs of TCA8113 siILK group. Xenograft tumor cells in TCA8113 siILK group were smaller and had less mitotic figures and karyoplasmic scale compared to the other 2 groups. The expression of p-Akt and p-GSK3 β in vitro and in vivo were obviously inhibited in TCA8113 siILK group compared The mean tumor mass was obviously smaller in TCA8113 siILK group than groups with a tumor inhibitory rate of 84% and 92%, respectively （ P 〈 0. with the other groups （P 〈 0.05 ）. the TCA8113 and TCA8113 vector 05）. Micro-blood vessel formation was also reduced in TCA8113 siILK group compared to the other ILK inhibits the growth of TCA8113 human tongue cancer tumor p-Akt and p-GSK313 as well as blood vessel formation.