中文摘要：

目的探讨人脑胶质瘤细胞系A172转染Atoc/i2基因后抑制细胞增殖情况及其机 制。方法将A172细胞分为空白对照组、转染空载质粒组（pcDNA3）、转染Notch2质粒组 （Notch2-pcDNA3）三组，后两组分别转染空载体和Notch2。采用MTT法检测其对细胞增殖的影响，流式细胞术检测其对细胞周期和凋亡的影响，Transwell方法检测其对细胞侵袭的作用，Western blotting检测转染Notch2质粒后A172细胞中重要信号通路成员Notch2、表皮生长因子受体 （EGFR）、组织磷酸化蛋白（p-AKT）、胞内磷脂酰肌醇激酶（PI3K）、人第10号染色体缺失的磷酸酶 （PTEN）、半胱氨酸天冬氨酸蛋白酶-3（caspase3）、细胞核因子kB（NF-kB）、增殖细胞核抗原（PCNA）、白细胞介素-2（Bcl-2）、基质金属蛋白酶2（MMP-2）、基质金属蛋白酶9（MMP-9）及周期素依赖性激酶 抑制因子l（CyclinDl）]相关基因的表达。结果MTT实验结果显示，与对照组及pcDNA3组比 较，A172细胞被转染Notch2后细胞存活率明显下降，差异有统计学意义（P〈0.05）;S期及G2/M期 细胞减少，G0/G1细胞较对照组相比增加22.1%,细胞明显被阻滞于G0/G1期；凋亡细胞数从对照组 的1.2%增加到14.8%;细胞侵袭数由对照组的35.23个降低至17.43个。与PI3K-AKT通路相关的 重要成员 EGFR、p-AKT、PI3K 以及 NF-kB、PCNA、Bc1-2、MMP-2、MMP-9 及 CyclinDl 等表达水平 均有明显下调；而拮抗PI3K/AKT活性的抑癌蛋白PTEN以及Caspase-3的表达则明显上调。结论转染TVoteM基因可抑制细胞增殖和侵袭，诱导细胞凋亡以及重要信号通路成员的基因表达变化。

英文摘要：

Objective To investigate the inhibitory effect of Notch! gene on the growth of A172 glioblastoma cells and its underlying mechanism. Methods Blank control group, empty vector transfection group （pcDNA3） and Notch2 plasmid transfection group （Notch2-pcDNA3） were employed in our study; A172 glioma cells in the later two groups were transfected with blank load plasmid and Notch2 plasmid, respectively. Cell growth was detected by MTT assay, and cell cycle and apoptosis were analyzed by flow cytometry. Transwell assay was used to study the cell invasion, and the expressions of important signaling pathway members,including Notch2, epidermal growth factor receptor （EGFR）, phospho-Akt （P-Akt）, phosphatidylinositol 3-kinase （PI3K）, phosphatase and tensin homologue deleted on chromosome 10 （PTEN）, caspase3, nuclear factor kB （NF-kB）, proliferating cell nuclear antigen （PCNA）, interleukin-2 （Bcl-2）,matrix metalloproteinase-2 （MMP-2）, MMP-9 and cyclin-dependent kinase inhibitor 1 （Cyclin Dl）, were detected by Western blotting. Results MTT assay showed that the cell viability in the A172 cells of Notch2-pcDNA3 group was significantly decreased as compared with that in the blank control cell and pcDNA3 groups （P〈0.05）; decreased cell number at S phase and G2/M phase was noted in A172 cells of Notch2-pcDNA3 group, while cell number at G0/G1 phaseincreased by 22.1% as compared with that in the blank control group; the percentage of apoptotic cells in the A172 cells of Notch2-pcDNA3 group （14.8%） was significantly increased as compared with that in the blank control cells （1.2%）; the number of invaded cells in the A172 cells of Notch2-pcDNA3 group （17.43） was significantly decreased as compared with that in the blank control cells （35.23）. The important members related to PI3K-AKT signaling pathway, including EGFR, p-AKT, PI3K, NF-KB, PCNA, Bcl-2, MMP-2, MMP-9 and Cyclin D1 had obvious decreased expression, while PTEN and Caspase-3, the antagonistic PI3K/AKT activi