垂体瘤转化基因抑制乳腺癌细胞的侵袭能力  

Pituitary tumor-transforming gene inhibits the invasion ability of breast cancer cells

作　　者：张红霞[1] 尹崇高[2] 李洪利[3] 孙永红[4] 

机构地区：[1]潍坊医学院基础医学院临床病理学系,山东潍坊261053 [2]潍坊医学院护理学院外科护理学教研室,山东潍坊261053 [3]潍坊医学院医学研究实验中心,山东潍坊261053 [4]潍坊医学院附属医院病理科,山东潍坊261041

出　　处：《肿瘤》2015年第10期1106-1112,共7页Tumor

摘　　要：目的 :探讨垂体瘤转化基因(pituitary tumor transforming gene,PTTG)在乳腺癌细胞侵袭中的作用。方法 :应用蛋白质印迹法检测PTTG蛋白在不同侵袭性乳腺癌细胞中的表达。将靶向PTTG的si RNA片段转染至高侵袭性乳腺癌MDA231细胞(命名为si PTTG/MDA231)后,应用蛋白质印迹法检测细胞中PTTG蛋白的表达水平;应用Transwell法检测si PTTG/MDA231细胞的侵袭能力;表皮细胞生长因子(epithelial growth factor,EGF)刺激si PTTG/MDA231细胞后,应用蛋白质印迹法检测细胞中磷酸化-Akt(phospho-Akt,p-Akt)和磷酸化-AMP相关蛋白激酶相关的蛋白激酶5[phospho-AMP-related protein kinase(AMPK)-related protein kinase 5,p-ARK5]的表达水平。结果 :高侵袭性乳腺癌MDA231细胞中PTTG蛋白的表达水平高于低侵袭性乳腺癌MCF7和T47-D细胞(P值均<0.05)。si PTTG/MDA231细胞中PTTG蛋白的表达水平低于空白对照组(MDA231细胞未进行任何转染)和阴性对照组(MDA231细胞转染阴性对照片段scrambling,命名为scr/MDA231细胞)(P值均<0.05)。si PTTG/MDA231细胞的侵袭能力低于空白对照组和阴性对照组(P值均<0.01)。EGF刺激0、5和10 min后,scr/MDA231细胞中p-Akt和p-ARK5蛋白的表达水平逐渐上调(P值均<0.05),而si PTTG/MDA231细胞中p-Akt和p-ARK5蛋白的表达水平无显著改变(P值均>0.05)。结论 :高侵袭性乳腺癌细胞中PTTG蛋白的表达水平较高。抑制PTTG的表达后,MDA231细胞的侵袭能力下降,这一作用可能与p-Akt和p-ARK5蛋白的表达调控有关。Objective： To explore the role of pituitary tumor-transforming gene （PTTG） in invasion of breast cancer cells.Methods： The expression level of PTTG protein in selected breast cancer cells with different invasion abilities was detected by Western blotting. The expression level of PTTG protein in MDA231 cells with high invasion ability after transfection with siRNA targeting PTTG （named as siPTTG/MDA231 cells） was detected by Western blotting. The invasion ability of siP-I-I-G/MDA231 cells was measured by Transwell cell invasion assay. The expression levels of phospho-Akt （p-Akt） and phospho-AMP-related protein kinase （AMPK）-related protein kinase 5 （p-ARK5） in siPTTG/MDA231 cells induced by epithelial growth factor （EGF） were examined by Western blotting. Results： The expression level of PTTG protein in MDA231 cells with high invasion ability was higher than those in MCF7 and T47-D cells with low invasion abilities （both P 〈 0.05）. The expression level of P-I-I-G protein in siPTTG/MDA231 cells was lower than that in MDA231 cells without any transfection or the cells transfected with scrambled fragment, which were named as scr/MDA231 cells （both P 〈 0.05）. The invasion ability of siPTTG/MDA231 was weakened as compared with those of the MDA231 cells without any transfection and the scr/MDA231 cells （both P 〈 0.01）. After treatment with EGF for 0, 5 and 10 min, the expression levels of p-Akt and p-ARK5 proteins in scr/MDA231 cells were obviously enhanced （all P 〈 0.05）, while the changes of expression levels of p-Akt and p-ARK5 proteins in siPTTG/MDA231 cells had no statistical significance （both P 〉 0.05）. Conclusion： The expression level of P-I-I-G protein in breast cancer cells with high invasion ability is high. The invasion ability of MDA231 cells after inhibition of PTTG expression is decreased, and this effect may be related to the regulation of expression levels of p-Akt and p-ARK5 proteins.

关 键 词：乳腺肿瘤 RNA 小分子干扰 肿瘤浸润 垂体瘤转化基因 

分 类 号：R737.9[医药卫生—肿瘤]