中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
CHINESE JOURNAL OF EXPERIMENTAL SURGERY
2015年
8期
1896-1898
,共3页
周闯%冯若%梁志伟%李仁峰%赵龙栓%翟文龙
週闖%馮若%樑誌偉%李仁峰%趙龍栓%翟文龍
주틈%풍약%량지위%리인봉%조룡전%적문룡
癌,肝细胞%高尔基体膜蛋白Ⅱ%上皮-间充质转化%转移
癌,肝細胞%高爾基體膜蛋白Ⅱ%上皮-間充質轉化%轉移
암,간세포%고이기체막단백Ⅱ%상피-간충질전화%전이
Carcinoma,hepatocellular%Golgi phosphoprotein 2%Eepithelial to mesenchymal transition%Metastasis
目的 探讨高尔基体膜蛋白Ⅱ(GOLPH2)促进人肝细胞肝癌(HCC)细胞上皮-间充质转化(EMT)转移复发的机制.方法 利用反转录-聚合酶链反应(RT-PCR)检测8种肝癌细胞株中GOLPH2的表达,选择其中高表达GOLPH2的MHCC-97H肝癌细胞利用慢病毒载体介导的RNA干扰GOLPH2的表达,观察侵袭、转移能力及EMT相关生物学特性是否因GOLPH2表达水平改变而发生变化.结果 RT-PCR结果显示GOLPH2的表达在HCC细胞株中随着恶性程度的增加而明显上升.在体外实验显示GOLPH2-RNA干扰(RNAi)转染组细胞克隆形成数(17.8±7.5)个显著低于对照组(41.7±5.3)个(P＜0.05).转染组及对照组发生迁移的细胞数分别为(27.8±11.6)个比(278.2±23.4)个(P＜0.01).转染组的迁移和侵袭能力明显减弱.同时转染组细胞间质表型N-钙黏蛋白(N-cadherin)和波形蛋白(Vimentin)下调而上皮表型E-钙黏蛋白(E-cadherin)、紧密连接蛋白-1(ZO-1)的表达上调(P＜0.01).结论 在HCC细胞中GLOPH2可通过调节EMT进而调控肝癌细胞侵袭转移.
目的 探討高爾基體膜蛋白Ⅱ(GOLPH2)促進人肝細胞肝癌(HCC)細胞上皮-間充質轉化(EMT)轉移複髮的機製.方法 利用反轉錄-聚閤酶鏈反應(RT-PCR)檢測8種肝癌細胞株中GOLPH2的錶達,選擇其中高錶達GOLPH2的MHCC-97H肝癌細胞利用慢病毒載體介導的RNA榦擾GOLPH2的錶達,觀察侵襲、轉移能力及EMT相關生物學特性是否因GOLPH2錶達水平改變而髮生變化.結果 RT-PCR結果顯示GOLPH2的錶達在HCC細胞株中隨著噁性程度的增加而明顯上升.在體外實驗顯示GOLPH2-RNA榦擾(RNAi)轉染組細胞剋隆形成數(17.8±7.5)箇顯著低于對照組(41.7±5.3)箇(P＜0.05).轉染組及對照組髮生遷移的細胞數分彆為(27.8±11.6)箇比(278.2±23.4)箇(P＜0.01).轉染組的遷移和侵襲能力明顯減弱.同時轉染組細胞間質錶型N-鈣黏蛋白(N-cadherin)和波形蛋白(Vimentin)下調而上皮錶型E-鈣黏蛋白(E-cadherin)、緊密連接蛋白-1(ZO-1)的錶達上調(P＜0.01).結論 在HCC細胞中GLOPH2可通過調節EMT進而調控肝癌細胞侵襲轉移.
목적 탐토고이기체막단백Ⅱ(GOLPH2)촉진인간세포간암(HCC)세포상피-간충질전화(EMT)전이복발적궤제.방법 이용반전록-취합매련반응(RT-PCR)검측8충간암세포주중GOLPH2적표체,선택기중고표체GOLPH2적MHCC-97H간암세포이용만병독재체개도적RNA간우GOLPH2적표체,관찰침습、전이능력급EMT상관생물학특성시부인GOLPH2표체수평개변이발생변화.결과 RT-PCR결과현시GOLPH2적표체재HCC세포주중수착악성정도적증가이명현상승.재체외실험현시GOLPH2-RNA간우(RNAi)전염조세포극륭형성수(17.8±7.5)개현저저우대조조(41.7±5.3)개(P＜0.05).전염조급대조조발생천이적세포수분별위(27.8±11.6)개비(278.2±23.4)개(P＜0.01).전염조적천이화침습능력명현감약.동시전염조세포간질표형N-개점단백(N-cadherin)화파형단백(Vimentin)하조이상피표형E-개점단백(E-cadherin)、긴밀련접단백-1(ZO-1)적표체상조(P＜0.01).결론 재HCC세포중GLOPH2가통과조절EMT진이조공간암세포침습전이.
Objective To explore the roles of golgi phosphoprotein 2 (GOLPH2) in hepatocellular carcinoma (HCC) metastatic progression as a promoter of epithelial to mesenchymal transition (EMT).Methods We evaluated the expression of GOLPH2 in 8 HCC cell lines using reverse transcriptase-polymerase chain reaction (RT-PCR).Lentiviral-mediated RNA interference was used to obtain a stable HCC cell line with low expression of GLOPH2.In vitro we also investigated the mechanisms of GLOPH2 in EMT metastasis in HCC cell lines.Results RT-PCR showed that the mRNA levels of GLOPH2 in high-metaststic HCC cell lines were significantly increased in comparison to low-metaststic ones.Clone formation experiment results showed clone formation number of RNAi transfection cells (17.8 ± 7.5) was significantly lower than that (41.7 ± 5.3) of control group (P ＜ 0.05).The number of migrating cells in low GOLPH2 expression group and control group was 27.8 ± 11.6 and 278.2 ± 23.4 respectively.In vitro,the characteristics of EMT were induced by lentivirus transduction of GOLPH2 into MHCC-97H cells,including the up-regulation of E-cadherin and ZO-1,and the concomitant down-regulation of N-cadherin and Vimentin.Conclusion Our findings have uncovered a novel role for GOLPH2 in HCC metastasis,and it may become the molecular targets for intervention of tumor metastasis.
