【摘要】 目的研究SMARCC1表达与脑胶质瘤临床指标和预后的相关性,及其对肿瘤细胞增殖和凋亡的影响。方法首先采用免疫组化实验检测SMARCC1在脑胶质瘤组织的表达,实验数据和临床指标及预后的相关性分析使用SPSS软件,P <0.05为有统计学意义。利用siRNA技术下调SMARCC1基因在脑胶质瘤细胞株的表达,利用MTT方法检测细胞增殖、Hochest/PI方法检测细胞凋亡,使用qPCR实验检测增殖和凋亡相关基因ki67和Bcl2的表达水平。实验数据采用GraphPad软件分析,P <0.05为有统计学意义。结果 SMARCC1表达分别和病理分级、复发等显著正相关,染色评分高的脑胶质瘤病人的总生存期和无病生存期都显著更短。使用siRNA技术下调SMARCC1的表达,随后观察到脑胶质瘤细胞株U251MG和U87MG的增殖显著降低而凋亡显著增加,同时,增殖和凋亡相关基因ki67和Bcl2的m RNA表达水平也出现下调。结论 SMARCC1过表达与脑胶质瘤的病理分级、复发及更差的预后显著相关。SMARCC1基因的下调能抑制脑胶质瘤细胞的增殖并促进凋亡,其机制可能与下调ki67和Bcl2的表达有关。更多还原

【Abstract】 Objective To study the correlation of SMARCC1 expression with clinical parameters and prognosis of glioma, and its effect on tumor cell proliferation and apoptosis. Methods The expression of SMARCC1 in glioma tissue was detected by immunohistochemistry. The correlation between experimental data and clinical indicators as well as prognosis was analyzed by SPSS software. Then, si RNA was used to down regulate the expression of SMARCC1 in glioma cell lines. MTT method was used to detect cell proliferation, Hochest/PI method was used to detect cell apoptosis, and qPCR experiment was used to detect the expression levels of ki67 and Bcl2 related to proliferation and apoptosis. The experimental data were analyzed by GraphPad software and P < 0.05 was statistically significant. Results The expression of SMARCC1 was positively correlated with pathological grade and recurrence. The overall survival and disease-free survival of patients with high IHC staining score were significantly shorter. si RNA was used to down regulate SMARCC1 expression, and then the proliferation of glioma cell lines U251 MG and U87 MG was decreased significantly, while the apoptosis was increased. At the same time, the mRNA expression levels of ki67 and Bcl2 were also down regulated. Conclusion The overexpression of SMARCC1 is significantly correlated with the pathological grade, recurrence and worse prognosis of glioma. Down regulation of SMARCC1 could inhibit the proliferation of glioma cells and promote apoptosis, which might be related to down-regulation of ki67 and Bcl2 expression.更多还原