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胶质瘤细胞中IL-1RAP的作用及其与STAT3的关系[J]. 肿瘤防治研究, 2015, 42(01): 23-27. DOI: 10.3971/j.issn.1000-8578.2015.01.006
引用本文: 胶质瘤细胞中IL-1RAP的作用及其与STAT3的关系[J]. 肿瘤防治研究, 2015, 42(01): 23-27. DOI: 10.3971/j.issn.1000-8578.2015.01.006
Role of IL-1RAP in Gliomas Cells and Its Relationship with STAT3[J]. Cancer Research on Prevention and Treatment, 2015, 42(01): 23-27. DOI: 10.3971/j.issn.1000-8578.2015.01.006
Citation: Role of IL-1RAP in Gliomas Cells and Its Relationship with STAT3[J]. Cancer Research on Prevention and Treatment, 2015, 42(01): 23-27. DOI: 10.3971/j.issn.1000-8578.2015.01.006

胶质瘤细胞中IL-1RAP的作用及其与STAT3的关系

Role of IL-1RAP in Gliomas Cells and Its Relationship with STAT3

  • 摘要: 目的 研究白介素1受体辅助蛋白(IL-1RAP)在胶质瘤中的作用及其与转录活化因子3(STAT3)的关系。方法 构建IL-1RAP表达载体,转染胶质瘤细胞系U251,利用流式±细胞仪检测转染IL-1RAP对U251细胞周期及凋亡影响。利用免疫共沉淀钓取STAT3,检测转染IL-1RAP后STAT3的表达情况,并利用免疫荧光方法检测IL-1RAP与STAT3的共定位情况。结果 IL-1RAP蛋白定位于胶质瘤细胞核。与转染空质粒对照组相比,IL-1RAP有明显的促进肿瘤细胞凋亡(52.10±5.51)% vs.(7.57± 0.54)%, P<0.05和周期阻滞作用(68.22±1.96)% vs.(38.31±7.22)%, P<0.05。通过免疫共沉淀和共定位证实IL-1RAP和STAT3可以相互作用。结论 IL-1RAP有抑制胶质瘤细胞增殖、促进细胞凋亡的作用。IL-1RAP可能通过与STAT3相互作用进入细胞核发挥促进细胞凋亡和抑制细胞周期的作用。

     

    Abstract: Objective To clarify the biological function of IL-1RAP in glioma cells and its relationship with signal transducer and activator of transcription 3(STAT3). Methods The glioma cell line U251was transfected with IL-1RAP expression vector. Cell cycle and apoptosis of IL-1RAP-transfected U251cells wereaanalyzed by flow cytometry. STAT3 expression was analyzed by immunocytochemistry and co-immunoprecipitation. Colocalization of IL-1RAP and STAT3 was detected by immunofluorescence. Results IL-1RAP protein was localized in the nucleus of glioma cells.Compared with control group transfected with empty plasmid, IL-1RAP transfection caused the apoptosis(52.10±5.51)% vs.(7.57±0.54)%, P<0.05 and cell cycle arrest of U251 cells(68.22±1.96)% vs.(38.31±7.22)%, P<0.05. In addition, IL-1RAP and STAT3 were colocalized and may interacted to affect the prognosis of glioma cells. Conclusion IL-1RAP could inhibit the proliferation and promote the apoptosis of glioma cells, which may be related with its interaction with STAT3.

     

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