国际肿瘤学杂志
國際腫瘤學雜誌
국제종류학잡지
JOURNAL OF INTERNATIONAL ONCOLOGY
2014年
5期
375-379
,共5页
梁宁%谢健%乔丽丽%张建东
樑寧%謝健%喬麗麗%張建東
량저%사건%교려려%장건동
食管肿瘤%半乳糖凝集素3%RNA过表达%生物学功能
食管腫瘤%半乳糖凝集素3%RNA過錶達%生物學功能
식관종류%반유당응집소3%RNA과표체%생물학공능
Esophageal neoplasms%Galectin 3%RNA over-expression%Biological function
目的 探讨半乳糖凝集素3(Gal3)对食管癌Eca109细胞增殖和转移的影响.方法 构建合成Gal3过表达慢病毒质粒转染食管癌Eca109细胞,应用倒置显微镜观察Gal3的过表达质粒转染食管癌细胞后荧光表达;CCK-8法检测转染前后细胞增殖能力的变化;用流式细胞术检测转染组细胞和未转染组细胞凋亡率.Transwell方法检测转染前后细胞迁移能力变化;用Western印迹检测Gal3转染前后在食管癌中表达水平变化.结果 Western印迹结果显示Gal3在食管癌细胞中表达,在Eca109/Gal3组中表达水平明显升高(t=14.33,P=0.013;t=10.28,P=0.037).CCK-8法检测发现转染后细胞增殖能力明显升高(t=-17.277,P＜0.05;t=-13.4,P＜0.05),流式细胞仪以Annexin-V/7-AAD双标法显示Eca109/Gal3组凋亡率明显下降(t=3.053,P＜0.05;=5.446,P＜0.05).Transwell实验结果,Eca109/Gal3组细胞转移率高于未转染组(t=3.465,P＜0.05;t=3.252,P＜0.05).结论 Gal3在食管癌细胞中有表达,并且其过表达能显著增强食管癌细胞的增殖、侵袭及迁移能力,明显抑制细胞的凋亡,深入研究Gal3可能为食管癌的治疗提供一种新的靶点.
目的 探討半乳糖凝集素3(Gal3)對食管癌Eca109細胞增殖和轉移的影響.方法 構建閤成Gal3過錶達慢病毒質粒轉染食管癌Eca109細胞,應用倒置顯微鏡觀察Gal3的過錶達質粒轉染食管癌細胞後熒光錶達;CCK-8法檢測轉染前後細胞增殖能力的變化;用流式細胞術檢測轉染組細胞和未轉染組細胞凋亡率.Transwell方法檢測轉染前後細胞遷移能力變化;用Western印跡檢測Gal3轉染前後在食管癌中錶達水平變化.結果 Western印跡結果顯示Gal3在食管癌細胞中錶達,在Eca109/Gal3組中錶達水平明顯升高(t=14.33,P=0.013;t=10.28,P=0.037).CCK-8法檢測髮現轉染後細胞增殖能力明顯升高(t=-17.277,P＜0.05;t=-13.4,P＜0.05),流式細胞儀以Annexin-V/7-AAD雙標法顯示Eca109/Gal3組凋亡率明顯下降(t=3.053,P＜0.05;=5.446,P＜0.05).Transwell實驗結果,Eca109/Gal3組細胞轉移率高于未轉染組(t=3.465,P＜0.05;t=3.252,P＜0.05).結論 Gal3在食管癌細胞中有錶達,併且其過錶達能顯著增彊食管癌細胞的增殖、侵襲及遷移能力,明顯抑製細胞的凋亡,深入研究Gal3可能為食管癌的治療提供一種新的靶點.
목적 탐토반유당응집소3(Gal3)대식관암Eca109세포증식화전이적영향.방법 구건합성Gal3과표체만병독질립전염식관암Eca109세포,응용도치현미경관찰Gal3적과표체질립전염식관암세포후형광표체;CCK-8법검측전염전후세포증식능력적변화;용류식세포술검측전염조세포화미전염조세포조망솔.Transwell방법검측전염전후세포천이능력변화;용Western인적검측Gal3전염전후재식관암중표체수평변화.결과 Western인적결과현시Gal3재식관암세포중표체,재Eca109/Gal3조중표체수평명현승고(t=14.33,P=0.013;t=10.28,P=0.037).CCK-8법검측발현전염후세포증식능력명현승고(t=-17.277,P＜0.05;t=-13.4,P＜0.05),류식세포의이Annexin-V/7-AAD쌍표법현시Eca109/Gal3조조망솔명현하강(t=3.053,P＜0.05;=5.446,P＜0.05).Transwell실험결과,Eca109/Gal3조세포전이솔고우미전염조(t=3.465,P＜0.05;t=3.252,P＜0.05).결론 Gal3재식관암세포중유표체,병차기과표체능현저증강식관암세포적증식、침습급천이능력,명현억제세포적조망,심입연구Gal3가능위식관암적치료제공일충신적파점.
Objective To investigate galectin3 on proliferation and migration of esophageal cancer Eca109 cells.Methods A lentiviral vector for over-expression of RNA targeting galectin3 was designed to transfect Eca109 cancer cells following plasmid-mediated transfection manual (Eca109/Gal3 cells).Inverted fluorescence microscope was used to observe the expression of EGFP.The proliferation of Eca109 cells was measured by cell counting Kit-8 assay.Eca109 cells apoptosis was determined by Annexin-V/7-AAD doublestaining.The migration capacity of Eca109 cells was determined in transwell assays.Western blot analysis was used to measure the expression of galectin3 protein.Results Galectin-3 expression was detected in Eca109 cells,with the Galectin3 expression in Eca109/Gal3 cells much more than non-transfected cells (t =14.33,P ＜ 0.05 ; t =10.28,P =0.037).Compared with non-transfected Eca109 cells,proliferation increased significantly in Eca109/Gal3 cells (t =-17.277,P ＜ 0.05 ; t =-13.4,P ＜ 0.05).Galectin3 evidently decreased in Eca109 cell apoptosis (t =3.053,P ＜ 0.05 ; t =5.446,P ＜ 0.05).Transwell migration assay showed that a greater number of Eca109/Gal3 cells crossed the artificial basement membrane compared with non-transfected Eca109 cells and negative control Eca109 cells (t =3.465,P ＜ 0.05; t =3.252,P ＜ 0.05).Conclusion Galectin3 expression is detected in transfected esophageal cancer Eca109 cells,whose overexpression can result in enhanced proliferation,migration,invasion as well as reduced apoptosis.These data indicate that in-depth research of galectin-3 may prove to be a potential molecular target for the treatment of esophageal cancer.
