中华血液学杂志
中華血液學雜誌
중화혈액학잡지
Chinese Journal of Hematology
2010年
6期
403-406
,共4页
薛雷喜%江淼%谢丽倩%阮长耿
薛雷喜%江淼%謝麗倩%阮長耿
설뢰희%강묘%사려천%원장경
硼替佐米%细胞迁移%血管内皮生长因子%膜联蛋白类
硼替佐米%細胞遷移%血管內皮生長因子%膜聯蛋白類
붕체좌미%세포천이%혈관내피생장인자%막련단백류
Bortezomib%Cell migration%Vascdor endothelial growth factor%Membrane associated proteins
目的 通过观察硼替佐米对内皮细胞迁移和血管新生相关因子表达的影响,探讨硼替佐米抗肿瘤细胞增殖作用的机制.方法 细胞计数法检测不同浓度硼替佐米分别处理12和24 h后内皮细胞系HMEC-1细胞的相对增殖活力;采用Transwell模型观察细胞迁移率;实时定量PCR方法检测Annexin A2、血管内皮生长因子(VEGF)基因表达水平,Western blot法检测Annexin A2在蛋白水平的变化.结果 2.5、5.0、10 nmol/L硼替佐米作用12 h,对HMEC-1细胞增殖抑制作用较弱[细胞增殖相对活力分别为(100.4±2.2)%、(79.3±2.1)%、(87.4±6.2)%],仅10 nmol/L组与对照组(100.O%)相比差异有统计学意义(P<0.05);但明显降低了细胞的迁移率,2.5、5.0、10.0 nmol/L硼替佐米组HMEC-1细胞迁移率分别为(69.7±6.0)%、(59.7±9.0)%、(54.7±12.7)%,与对照组(100.0%)相比,差异均具有统计学意义(P<0.05):硼替佐米抑制了Annexin A2和VEGF基因的表达,5.0 nmol/L硼替佐米处理12 h,HMEC-1细胞Annexin A2和VEGF相对表达水平分别为0.540±0.001和0.673±0.153,与对照组(均设定为1.000)相比,差异均有统计学意义(P<0.05),Western blot同样显示Annexin A2在蛋白水平表达下调.结论 硼替佐米可通过下调 Annexin A2和VEGF的表达,从而抑制内皮细胞系HMEC-1细胞的迁移.
目的 通過觀察硼替佐米對內皮細胞遷移和血管新生相關因子錶達的影響,探討硼替佐米抗腫瘤細胞增殖作用的機製.方法 細胞計數法檢測不同濃度硼替佐米分彆處理12和24 h後內皮細胞繫HMEC-1細胞的相對增殖活力;採用Transwell模型觀察細胞遷移率;實時定量PCR方法檢測Annexin A2、血管內皮生長因子(VEGF)基因錶達水平,Western blot法檢測Annexin A2在蛋白水平的變化.結果 2.5、5.0、10 nmol/L硼替佐米作用12 h,對HMEC-1細胞增殖抑製作用較弱[細胞增殖相對活力分彆為(100.4±2.2)%、(79.3±2.1)%、(87.4±6.2)%],僅10 nmol/L組與對照組(100.O%)相比差異有統計學意義(P<0.05);但明顯降低瞭細胞的遷移率,2.5、5.0、10.0 nmol/L硼替佐米組HMEC-1細胞遷移率分彆為(69.7±6.0)%、(59.7±9.0)%、(54.7±12.7)%,與對照組(100.0%)相比,差異均具有統計學意義(P<0.05):硼替佐米抑製瞭Annexin A2和VEGF基因的錶達,5.0 nmol/L硼替佐米處理12 h,HMEC-1細胞Annexin A2和VEGF相對錶達水平分彆為0.540±0.001和0.673±0.153,與對照組(均設定為1.000)相比,差異均有統計學意義(P<0.05),Western blot同樣顯示Annexin A2在蛋白水平錶達下調.結論 硼替佐米可通過下調 Annexin A2和VEGF的錶達,從而抑製內皮細胞繫HMEC-1細胞的遷移.
목적 통과관찰붕체좌미대내피세포천이화혈관신생상관인자표체적영향,탐토붕체좌미항종류세포증식작용적궤제.방법 세포계수법검측불동농도붕체좌미분별처리12화24 h후내피세포계HMEC-1세포적상대증식활력;채용Transwell모형관찰세포천이솔;실시정량PCR방법검측Annexin A2、혈관내피생장인자(VEGF)기인표체수평,Western blot법검측Annexin A2재단백수평적변화.결과 2.5、5.0、10 nmol/L붕체좌미작용12 h,대HMEC-1세포증식억제작용교약[세포증식상대활력분별위(100.4±2.2)%、(79.3±2.1)%、(87.4±6.2)%],부10 nmol/L조여대조조(100.O%)상비차이유통계학의의(P<0.05);단명현강저료세포적천이솔,2.5、5.0、10.0 nmol/L붕체좌미조HMEC-1세포천이솔분별위(69.7±6.0)%、(59.7±9.0)%、(54.7±12.7)%,여대조조(100.0%)상비,차이균구유통계학의의(P<0.05):붕체좌미억제료Annexin A2화VEGF기인적표체,5.0 nmol/L붕체좌미처리12 h,HMEC-1세포Annexin A2화VEGF상대표체수평분별위0.540±0.001화0.673±0.153,여대조조(균설정위1.000)상비,차이균유통계학의의(P<0.05),Western blot동양현시Annexin A2재단백수평표체하조.결론 붕체좌미가통과하조 Annexin A2화VEGF적표체,종이억제내피세포계HMEC-1세포적천이.
Objective To investigate the effects of bortezomib on the migration of endothelial cells and the expression of angiogenesis-related molecules,and explore the mechanism of its antiproliferation of tumor cells.Methods Cell count kit CCK-8 was used to detect the relative proliferation activity of cells after treated by bortezomib at different concentrations for 12 h and 24 h,respectively.Transwell model was uesd to detect the migration rate of cells.Expression levels of VEGF and Annexin A2 genes were determined by realtime quantitative PCR.Annexin A2 protein was validated by Western blot.Results After treated with bertezomib at concentrations of 2.5、5.0 and 10 nmol/L for 12h,respectively,the HMEC-1 cell proliferation activity was 1.004±0.002,0.793±0.021 and 0.874 4-0.062,respectively,being no statistical difference from that of control group(1.000)P<0.05);while the migration rates of them were 0.697±0.060,0.597±0.090 and 0.874±0.062,respectively,being significantly lower than that of control group(1.000)(P<0.05 ) and so did for the expression of VEGF and Annexin A2 genes.After treated with 5 nmol/L bortezomib for 12 h.the Annexin A2 and VEGF gene relative expression level of HMEC-1 cells was 0.540±0.001 and 0.793±0.153,respectively,being of statistical difference from that of control group(1.000)P<0.05).The conspicuous downregulation of Annexin A2 protein was also confirmed by Western Blot.Conclusions Bortezomib can inhibit migration of endothelial cell HMEC-1 by downregulating the expression of VEGF and Annexin A2, displaying a new mechanism of bortezomib for inhibition of tumor proliferation.
