CAJ | 학술논문

目的观察Vasostatin基因表达对胰腺癌内皮细胞迁移能力的影响.方法应用不同浓度的载有Vasostatin基因的腺病毒(Ad-vasosiatin)感染胰腺癌内皮细胞,以Ad-lacZ感染及磷酸盐缓冲液(PBS)作为对照组.应用损伤修复、Transwell小室、小管形成3种不同方法观察胰腺癌内皮细胞迁移能力的变化及其与感染病毒的量效关系.结果培养48 h后,PBS组与Ad-lacZ组的划痕损伤区域几乎完全恢复；而Ad-vasostatin组的划痕损伤区域无明显恢复.以MOI 1、2、5感染细胞,Ad-lacZ组的迁移率分别为(84.7±2.6)％、(80.7±1.7)％和(81.3±4.0)％；Ad-vasostatin组为(77.7±2.1)％、(67.3±2.1)％和(38.8±2.1)％,Ad-vasostatin呈剂量依赖性抑制细胞迁移率,MOI=5时的细胞迁移率大幅度降低(F=180.88,P＜0.05).以MOI1、5、10感染时,Ad-lacZ组的小管形成数分别为(118±6)、(120±6)、(82±5)个；Ad-vasostatin组为(65±4)、(21±4)、(4±1)个,Ad-vasostatin呈剂量依赖性抑制胰腺癌内皮细胞的小管形成,在MOI=10时已很难形成管状结构(F =300.85,P＜0.05).结论 Vasostatin基因能显著抑制胰腺癌内皮细胞的体外迁移能力,且呈剂量依赖性.
목적 관찰Vasostatin기인표체대이선암내피세포천이능력적영향.방법 응용불동농도적재유Vasostatin기인적선병독(Ad-vasosiatin)감염이선암내피세포,이Ad-lacZ감염급린산염완충액(PBS)작위대조조.응용손상수복、Transwell소실、소관형성3충불동방법관찰이선암내피세포천이능력적변화급기여감염병독적량효관계.결과 배양48 h후,PBS조여Ad-lacZ조적화흔손상구역궤호완전회복；이Ad-vasostatin조적화흔손상구역무명현회복.이MOI 1、2、5감염세포,Ad-lacZ조적천이솔분별위(84.7±2.6)％、(80.7±1.7)％화(81.3±4.0)％；Ad-vasostatin조위(77.7±2.1)％、(67.3±2.1)％화(38.8±2.1)％,Ad-vasostatin정제량의뢰성억제세포천이솔,MOI=5시적세포천이솔대폭도강저(F=180.88,P＜0.05).이MOI1、5、10감염시,Ad-lacZ조적소관형성수분별위(118±6)、(120±6)、(82±5)개；Ad-vasostatin조위(65±4)、(21±4)、(4±1)개,Ad-vasostatin정제량의뢰성억제이선암내피세포적소관형성,재MOI=10시이흔난형성관상결구(F =300.85,P＜0.05).결론 Vasostatin기인능현저억제이선암내피세포적체외천이능력,차정제량의뢰성.
Objective To investigate the effect of vasostatin on the migration of pancreatic cancer endothelial cells.Methods Ad-vasostatin with different concentrations of vasostatin was used to transfect pancreatic cancer endothelial cells.Ad-LacZ transfection and PBS was used as control.The effect of vasostatin gene mediated by adenovirus on the migration of pancreatic cancer endothelial cells was measured by woundhealing assay,transwell migration assay,and tube formation assay.Results The scratched lines in PBS group and Ad-LacZ group were almost healed 48 hours later,while the lines in Ad-vasostatin group were rarely healed.At the MOI of 1,2,5,the migration rate of Ad-Laz group was ( 84.7 ± 2.6) ％,(80.7 ± 1.7 ) ％ and (81.3±4.0)％,while the corresponding values were (77.7 ±2.1)％,(67.3 ±2.1)％ and (38.8 ±2.1 ) ％ in Ad-vasostatin group.Transwell migration assay indicated that the number of migrated cells in Advasostatin group was inhibited in a dose-dependant manner,at the MOI of 5,the migration became significantly decreased (F=180.88,P ＜0.05).At the MOI of 1,5,10,the number of tubes in Ad-LacZ group was 118±6,120±6 and 82±5,while the corresponding values were 65±4,21±4 and 4 ±1 in Ad-vasostatin group.The number of tubes of pancreatic cancer endothelial cells was inhibited by Ad-vasostatin in a dose-dependant manner,at the MOI of 10, it was difficult to form the tubes (F-300.85,P＜0.05). Conclusions The vasostatin gene mediated by adenovirus has a significant inhibitory effect on the migation of pancreatic cancer endothelial cells in vitro in a dose-dependent manner.