摘要
目的:检测磷酸化应激诱导蛋白1(stress-induced phosphoprotein 1,STIP1)在胶质瘤组织和正常脑组织中的表达差异,探讨STIP1对胶质瘤细胞株U87、U251细胞增殖、凋亡及侵袭能力的影响。方法:运用实时定量聚合酶链式反应(qRT-PCR)、免疫组化及蛋白印迹检测胶质瘤组织和正常脑组织中STIP1的表达;小干扰RNA(STIP1-siRNA)转染U87、U251细胞株后,使用噻唑蓝(MTT)法、流式细胞仪和Transwell小室观察细胞的增殖、凋亡和侵袭能力。结果:STIP1在胶质瘤Ⅳ级组织中的表达明显高于正常脑组织,但在胶质瘤Ⅱ、Ⅲ级中的表达与正常脑组织无明显差异。U87、U251细胞株转染STIP1-siRNA后,细胞增殖和侵袭能力明显受到抑制,而细胞凋亡率明显上升。结论:STIP1在胶质母细胞瘤组织中高表达,下调STIP1可以抑制胶质瘤细胞株U87和U251的增殖,阻滞细胞周期,促进其细胞凋亡,并可抑制其侵袭力。
Objective:To investigate the expression difference of stress-induced phosphoprotein 1(STIP1)in glioma tissues and normal brain tissues,and its effects on proliferation,apoptosis and invasion of glioma cell lines(U87 and U251).Methods:Real-time quantitative polymerase chain reaction(qRT-PCR),immunohistochemistry,and Western blot were used to detect the expression of STIP1 in glioma tissues and normal brain tissues.Small interfering RNA(STIP1-siRNA)was used to transfect U87 and U251 cell lines.Then the effects of cell proliferation,apoptosis and invasion were observed by MTT method,flow cytometry and Transwell chamber.Results:The expression of STIP1 in glioma gradeⅣtissues was significantly higher than in non-tumor brain tissues,but it was not significantly different between glioma gradeⅡandⅢand non-tumor brain tissues.After U87 and U251 cell lines were transfected with STIP1-siRNA,the cell proliferation and invasion ability were significantly inhibited,and the apoptosis rate was increased significantly.Conclusion:STIP1 is highly expressed in glioblastoma tissues.Down-regulating STIP1 can inhibit the proliferation of glioma cell lines U87 and U251,block the cell cycle,promote its apoptosis,and inhibit its invasiveness.
作者
赵安静
殷洪伟
李学涛
孙春明
ZHAO Anjing;YIN Hongwei;LI Xuetao;SUN Chunming(Department of Oncology,Changhai Hospital,the Naval Military Medical University,Shanghai 200433,China;Neurosurgery Department and Brain and Nerve Research Laboratory,the First Affiliated Hospital of Soochow University,Jiangsu Suzhou 215006,China)
出处
《现代肿瘤医学》
CAS
2020年第21期3661-3665,共5页
Journal of Modern Oncology