CAJ | 학술논문

背景与目的：研究证实垂体肿瘤转化基因1(pituitary tumor transforming gene 1，PTTG1)的表达情况与各类肿瘤细胞的恶性程度有关，但是其在胶质瘤中的作用尚不清楚。本研究旨在探讨PTTG1在恶性胶质瘤侵袭中的作用及其临床意义。方法：应用蛋白质印迹法(Western blot)检测PTTG1蛋白在不同胶质瘤细胞系中的表达；采用小RNA质粒干扰技术抑制U87细胞中PTTG1蛋白的表达，应用Western blot技术检测转染的效率；通过体外侵袭实验检测转染后细胞侵袭力的变化；采用Western blot技术检测经过表皮细胞生长因子(epithelial growth factor，EGF)刺激后敲除PTTG1的细胞组(siPTTG1/U87)与转染空载的细胞组(Scr/U87)中Akt、ARK5磷酸化的情况。结果：PTTG1蛋白在各恶性胶质瘤细胞系中均高表达；敲除PTTG1后U87细胞的侵袭力明显下降；对Scr/U87细胞进行EGF刺激5 min后，Akt、ARK5的磷酸化情况显著增强，而无论有无EGF的刺激，siPTTG1/U87中Akt、ARK5的磷酸化情况都没有明显改变。结论：在恶性胶质瘤细胞中，PTTG1蛋白呈高表达状态并且与侵袭性显著相关，其对侵袭性的调控可能是通过Akt-ARK5通路实现的。
배경여목적：연구증실수체종류전화기인1(pituitary tumor transforming gene 1，PTTG1)적표체정황여각류종류세포적악성정도유관，단시기재효질류중적작용상불청초。본연구지재탐토PTTG1재악성효질류침습중적작용급기림상의의。방법：응용단백질인적법(Western blot)검측PTTG1단백재불동효질류세포계중적표체；채용소RNA질립간우기술억제U87세포중PTTG1단백적표체，응용Western blot기술검측전염적효솔；통과체외침습실험검측전염후세포침습력적변화；채용Western blot기술검측경과표피세포생장인자(epithelial growth factor，EGF)자격후고제PTTG1적세포조(siPTTG1/U87)여전염공재적세포조(Scr/U87)중Akt、ARK5린산화적정황。결과：PTTG1단백재각악성효질류세포계중균고표체；고제PTTG1후U87세포적침습력명현하강；대Scr/U87세포진행EGF자격5 min후，Akt、ARK5적린산화정황현저증강，이무론유무EGF적자격，siPTTG1/U87중Akt、ARK5적린산화정황도몰유명현개변。결론：재악성효질류세포중，PTTG1단백정고표체상태병차여침습성현저상관，기대침습성적조공가능시통과Akt-ARK5통로실현적。
Background and purpose:Numerous researches indicated that the expression of pituitary tumor transforming gene1 (PTTG1) was correlated with the severity of glioma tumors. However the specific mechanism of PTTG1 is not clear in glioma. In this study, we explored the role and significance of PTTG1 in the invasion of glioma cells. Methods:Western blot was used to detect the expression of PTTG1 protein in various glioma cell lines. siRNA plasmid was used to transfect U87 cells. Western blot was used to analyze the expression of PTTG1 protein in transfected U87 cells. Matrigel invasion assay was used to detect the invasive ability in the cells being transfected in vitro. Western blot was used to analyze epithelial growth factor (EGF) induced protein phosphorylation of ARK5 and Akt in the cells being transfected PTTG1 plasmid (siPTTG1/U87) and scrambled siRNA (Scr/U87). Results:The expression of PTTG1 protein was higher in all glioma cell lines. After transfection, the invasion of siPTTG1/U87 was obviously decreased after 5 min with EGF stimulation than the Scr/U87, the phosphorylation of ARK5 and Akt was significantly enhanced. However, whether or not the existence of EGF, the phosphorylation of ARK5 and Akt had no differences in siPTTG1/U87. Conclusion:In glioma cells, PTTG1 protein is high expressed and maybe have an important function in glioma cells invasion through Akt-ARK5 signaling pathway.