中文摘要：

目的研究对Tb舌癌细胞的整合素连接激酶（ILK）进行特异性siRNA沉默后,下游信号分子Akt、GSK3β磷酸化状态及对移植瘤生长和自发性转移的变化。方法建立特异性si ILK表达载体和无同源性的对照载体,通过Lipofectamine 2000介导稳定转染人舌鳞癌Tb细胞,然后将Tb、Tb vector和Tb silk 3组细胞分别注入裸鼠皮下构建移植瘤模型,5周后检测瘤大小和质量,对裸鼠肺及瘤组织行常规病理学检查,用免疫荧光技术检测癌细胞的p-Akt和p-GSK3β等的表达,并对瘤组织内血管生成情况进行观察。结果 Tb组、Tb vector组肺组织均发现自发性转移瘤,Tb si ILK组肺组织未发现自发性转移瘤;Tb si ILK组移植瘤细胞形态较其他二组体积减小,核分裂相较少,核质比例缩小;Tb si ILK组在体内和体外实验中的p-Akt和p-GSK3β表达较其他二组均明显下降;Tb si ILK组移植瘤质量（1.68±1.35）g较Tb组（3.58±1.04）g与Tb vector组（3.64±0.65）g分别降低了53.0%和53.8%（P〈0.05）;Tb si ILK组移植瘤血管[（5.6±2.2）/视野]生成较Tb组[（15.3±2.3）/视野]和Tb vector组[（14.6±1.4）/视野]也明显减少（P〈0.05）。结论特异性ILK表达沉默抑制Tb舌癌移植瘤的血管生成和瘤细胞增殖,可能与其抑制下游信号传导分子Akt及GSK3β的磷酸化有关,提示ILK有望成为肿瘤治疗的靶基因。

英文摘要：

Objective To investigate the effects of silencing integrin-linked kinase in Tb human tongue cancer cell on the expression and phosphorylation of its downstream signal molecular Akt and GSK3 β and growth and spontaneous metastasis of tumor xenografts. Methods Target cells were constructed by transfecting specific si ILK plasmid and a non-homologous vector negative control into Tb cells. Tb,Tb vector and Tb si ILK cells,respectively,were injected into nude mice subcutaneously. Weight and size of the xenograft tumor from nude mice weremeasured. Morphology of tumor tissue was observed by routine pathology methods. Changes in the expression and phosphorylation of Akt and GSK3β and micro-blood vessels in tumor tissue were detected by immunofluorescence and laser scanning confocal detection,respectively. Results Phosphorylation of Akt and GSK3β in vivo and in vitro was obviously inhibited in Tb si ILK group compared with the other groups. Compared with Tb [（ 3. 58 ± 1. 04） g]and Tb vector [（ 3. 64 ± 0. 65） g]group,the mean tumor mass in Tb si ILK group [（ 1. 68 ± 1. 35） g]decreased53. 0% and 53. 8%,respectively（ P 0. 05）. Microvessel formation was also reduced in Tb si ILK group compared to the other groups（ P 0. 05）. Conclusions Silencing ILK inhibits proliferation and microvessel formation of Tb human tongue cancer tumor xenograft,which may be related with the inhibition of phosphorylation of Akt and GSK3β. The results suggest that ILK is a potential therapeutic target protein for tongue cancer.