疑难病杂志
疑難病雜誌
의난병잡지
JOURNAL OF DIFFICULT AND COMPLICATED CASES
2014年
5期
506-508,512
,共4页
肝癌%HBx-Hep G2 细胞%三氧化二砷%黏附%侵袭%CD44拼接异构体6
肝癌%HBx-Hep G2 細胞%三氧化二砷%黏附%侵襲%CD44拼接異構體6
간암%HBx-Hep G2 세포%삼양화이신%점부%침습%CD44병접이구체6
Liver cancer%HBx-Hep G2%Arsenic trioxide%Adhesion%Invasion%CD44 splice isoforms 6
目的：探讨三氧化二砷（ As2 O3）对HBx-Hep G2细胞体外黏附、侵袭、迁移能力的影响及其机制。方法慢病毒介导构建HBx-Hep G2细胞模型，免疫细胞化学法检测HBx蛋白表达，分别采用MTT法、Transwell小室检测As2 O3对HBx-Hep G2细胞黏附、迁移、侵袭能力的影响，免疫组化方法检测As2 O3作用前后HBx-Hep G2细胞CD44V6表达的改变。结果构建后的HBx-Hep G2细胞呈现HBx阳性信号，主要分布于胞浆，无局部高浓度聚集。随着As2 O3作用时间的延长及浓度增加，HBx-Hep G2细胞对Matrigel的黏附能力也随之增加；与作用前相比，As2 O3作用后HBx-Hep G2细胞游走与穿透基底膜的能力明显受抑制[（128±8）vs．（102±7）、（96±5）vs．（85±6）]个/HP （ P ＜0创．05）；与As2O3作用前比较，H-SCOKE 及阴性表达率均下降[（3．75±0．55） vs．（2．54±0．68）、（92．65±4．86）％vs．（63．27±5．98）％]能抑制HBx-Hep G2细胞CD44v6的表达（ P ＜0．05）。结论 As2 O3能抑制HBx-Hep G2细胞与细胞的黏附、迁移和侵袭能力，其抑制作用可能与CD44v6的表达下调有关。
目的：探討三氧化二砷（ As2 O3）對HBx-Hep G2細胞體外黏附、侵襲、遷移能力的影響及其機製。方法慢病毒介導構建HBx-Hep G2細胞模型，免疫細胞化學法檢測HBx蛋白錶達，分彆採用MTT法、Transwell小室檢測As2 O3對HBx-Hep G2細胞黏附、遷移、侵襲能力的影響，免疫組化方法檢測As2 O3作用前後HBx-Hep G2細胞CD44V6錶達的改變。結果構建後的HBx-Hep G2細胞呈現HBx暘性信號，主要分佈于胞漿，無跼部高濃度聚集。隨著As2 O3作用時間的延長及濃度增加，HBx-Hep G2細胞對Matrigel的黏附能力也隨之增加；與作用前相比，As2 O3作用後HBx-Hep G2細胞遊走與穿透基底膜的能力明顯受抑製[（128±8）vs．（102±7）、（96±5）vs．（85±6）]箇/HP （ P ＜0創．05）；與As2O3作用前比較，H-SCOKE 及陰性錶達率均下降[（3．75±0．55） vs．（2．54±0．68）、（92．65±4．86）％vs．（63．27±5．98）％]能抑製HBx-Hep G2細胞CD44v6的錶達（ P ＜0．05）。結論 As2 O3能抑製HBx-Hep G2細胞與細胞的黏附、遷移和侵襲能力，其抑製作用可能與CD44v6的錶達下調有關。
목적：탐토삼양화이신（ As2 O3）대HBx-Hep G2세포체외점부、침습、천이능력적영향급기궤제。방법만병독개도구건HBx-Hep G2세포모형，면역세포화학법검측HBx단백표체，분별채용MTT법、Transwell소실검측As2 O3대HBx-Hep G2세포점부、천이、침습능력적영향，면역조화방법검측As2 O3작용전후HBx-Hep G2세포CD44V6표체적개변。결과구건후적HBx-Hep G2세포정현HBx양성신호，주요분포우포장，무국부고농도취집。수착As2 O3작용시간적연장급농도증가，HBx-Hep G2세포대Matrigel적점부능력야수지증가；여작용전상비，As2 O3작용후HBx-Hep G2세포유주여천투기저막적능력명현수억제[（128±8）vs．（102±7）、（96±5）vs．（85±6）]개/HP （ P ＜0창．05）；여As2O3작용전비교，H-SCOKE 급음성표체솔균하강[（3．75±0．55） vs．（2．54±0．68）、（92．65±4．86）％vs．（63．27±5．98）％]능억제HBx-Hep G2세포CD44v6적표체（ P ＜0．05）。결론 As2 O3능억제HBx-Hep G2세포여세포적점부、천이화침습능력，기억제작용가능여CD44v6적표체하조유관。
Objective To evaluate the effect of arsenic trioxide ( As2 O3 ) on HBx-Hep G2 cells in vitro adhesion , in-vasion and migration of its mechanism .Methods HBx-Hep G2 cell model were built by lentivirus-mediated , immunocyto-chemistry assay protein HBx, respectively, using the MTT assay , Transwell chamber detection As2O3's effect on HBx-Hep G2 cell adhesion, migration, invasion ability was detected.The role of As2O3 on HBx-Hep G2 cells CD44V6 expression changes were detected by immunohistochemistry .Results After built, HBx-Hep G2 cells showed positive HBx signals , mainly distrib-uted in the cytoplasm , no local high concentration of aggregation .With the increase of As 2 O3 to extend the role of time and concentration, HBx-Hep G2 cells on matrigel adhesion capacity also increased; compared with the previous , after using of As2 O3 , HBx-Hep G2 and penetrate the basement membrane of the cell migration was markedly inhibited [ ( 128 ±8 ) vs. (102 ±7),(96 ±5)vs.(85 ±6)] /HP ( P <0.05);compared with before As2O3 effects, H-SCOKE rate and negative ex-pression were decreased [(3.75 ±0.55)vs.(2.54 ±0.68),(92.65 ±4.86)%vs.(63.27 ±5.98)%].It can inhibit the ex-pression of CD44v6 HBx-Hep G2( P <0.05).Conclusion As2O3 can inhibit HBx-Hep G2 cell-cell adhesion, migration and invasion, and its inhibition may be associated with down-regulation of the expression of CD 44v6.
