中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
Chinese Journal of Experimental Surgery
2015年
11期
2629-2631
,共3页
向丹%郑富霖%李明%提爱军%张龙%李文岗
嚮丹%鄭富霖%李明%提愛軍%張龍%李文崗
향단%정부림%리명%제애군%장룡%리문강
胆管癌%第10号染色体缺失的磷酸酶和张力蛋白的同源基因%上皮-间充质转化
膽管癌%第10號染色體缺失的燐痠酶和張力蛋白的同源基因%上皮-間充質轉化
담관암%제10호염색체결실적린산매화장력단백적동원기인%상피-간충질전화
Cholangiocarcinoma%Phosphatase and tensin homolog deleted on chromosome 10%Epithelial-mesenchymal transition
目的 探讨第10号染色体缺失的磷酸酶和张力蛋白的同源基因(PTEN)对胆管癌细胞株QBC939迁移能力的抑制作用及其机制.方法 取4μg PTEN质粒转染胆管癌细胞株QBC939,转染72 h后,采用Transwell迁移实验和Western blot检测上调PTEN对QBC939细胞迁移能力和上皮-间充质转化(EMT)中重要的分子标志物表达的影响.结果 人胆管癌细胞株QBC939经PTEN质粒转染72 h后,其通过基质膜细胞数目比较对照组数目减半(P<0.01),迁移能力减弱,与EMT相关分子标志物Slug、Snail、波形蛋白(Vimentin)蛋白表达水平降低,磷酸肌醇3激酶(PI3K)/蛋白激酶B(Akt)信号通路中的磷酸化Akt (p-Akt)蛋白表达也明显减少.结论 PTEN可以通过抑制EMT进而影响胆管癌细胞迁移,PTEN对EMT的抑制作用可能是由PI3K/Akt信号通路调节的.
目的 探討第10號染色體缺失的燐痠酶和張力蛋白的同源基因(PTEN)對膽管癌細胞株QBC939遷移能力的抑製作用及其機製.方法 取4μg PTEN質粒轉染膽管癌細胞株QBC939,轉染72 h後,採用Transwell遷移實驗和Western blot檢測上調PTEN對QBC939細胞遷移能力和上皮-間充質轉化(EMT)中重要的分子標誌物錶達的影響.結果 人膽管癌細胞株QBC939經PTEN質粒轉染72 h後,其通過基質膜細胞數目比較對照組數目減半(P<0.01),遷移能力減弱,與EMT相關分子標誌物Slug、Snail、波形蛋白(Vimentin)蛋白錶達水平降低,燐痠肌醇3激酶(PI3K)/蛋白激酶B(Akt)信號通路中的燐痠化Akt (p-Akt)蛋白錶達也明顯減少.結論 PTEN可以通過抑製EMT進而影響膽管癌細胞遷移,PTEN對EMT的抑製作用可能是由PI3K/Akt信號通路調節的.
목적 탐토제10호염색체결실적린산매화장력단백적동원기인(PTEN)대담관암세포주QBC939천이능력적억제작용급기궤제.방법 취4μg PTEN질립전염담관암세포주QBC939,전염72 h후,채용Transwell천이실험화Western blot검측상조PTEN대QBC939세포천이능력화상피-간충질전화(EMT)중중요적분자표지물표체적영향.결과 인담관암세포주QBC939경PTEN질립전염72 h후,기통과기질막세포수목비교대조조수목감반(P<0.01),천이능력감약,여EMT상관분자표지물Slug、Snail、파형단백(Vimentin)단백표체수평강저,린산기순3격매(PI3K)/단백격매B(Akt)신호통로중적린산화Akt (p-Akt)단백표체야명현감소.결론 PTEN가이통과억제EMT진이영향담관암세포천이,PTEN대EMT적억제작용가능시유PI3K/Akt신호통로조절적.
Objective To investigate the effects of phosphatase and tensin homolog deleted on chromosome 10 (PTEN) on cholangiocarcinoma cell QBC939 migration and the mechanisms by which PTEN regulates QBC939 cell migration.Methods QBC939 cells were transfected with 4 μg PTEN-expression vector for 72 h.Transwell assay was used to detect the effects of PTEN on cholangiocarcinoma cell migration.Western blotting was used to determine the protein levels involving in epithelial-mesenchymal transition (EMT) and phosphatidylinositol 3 kinase (PI3K)/protein kinase B (Akt) signaling pathway after PTEN was overexpressed in QBC939 cells.Results Overexpression of PTEN inhibited cholangiocarcinoma cell QBC939 migration as demonstrated by decreasing the ability of cells to migrate through the membrance in the Transwell migration assay (P < 0.01).The enforced expression of PTEN inhibited EMT of QBC939 cells as demonstrated by decreasing Slug, Snail and Vimentin protein expression.In addition, upregulation of PTEN inhibited phosphorylation of Akt.Conclusion These results suggest PTEN inhibited cell migration through regulating EMT process in QBC939 cells;PTEN inhibited EMT process of QBC939 cells by inactivating the PI3K/Akt signal pathway.