中国病理生理杂志
中國病理生理雜誌
중국병리생리잡지
CHINESE JOURNAL OF PATHOPHYSIOLOGY
2014年
4期
620-624
,共5页
曹稳珑%韦尉元%张笑石%罗文%严林海%谢玉波%肖强
曹穩瓏%韋尉元%張笑石%囉文%嚴林海%謝玉波%肖彊
조은롱%위위원%장소석%라문%엄림해%사옥파%초강
胃肿瘤%SGC-7901细胞%转录因子CDX2
胃腫瘤%SGC-7901細胞%轉錄因子CDX2
위종류%SGC-7901세포%전록인자CDX2
Stomach neoplasms%SGC-7901 cells%Transcription factor CDX2
目的:探索CDX2过表达对人胃癌SGC-7901细胞增殖、生长和细胞周期的影响及其分子机制。方法:采用携带CDX2基因的重组慢病毒颗粒( LV-CDX2-GFP)感染SGC-7901细胞,作为实验组( LV-CDX2-GFP组);以对照慢病毒颗粒( LV-GFP)感染SGC-7901细胞,作为阴性对照组( LV-GFP组);空白对照组常规培养,不做任何处理。分别采用CCK-8法检测细胞的增殖活力,流式细胞术检测各组细胞周期的分布,半定量逆转录-聚合酶链反应( RT-PCR)和Western blotting 技术检测细胞中CDX2、Bax、Bcl-2、cyclin D1和survivin mRNA和蛋白的表达。结果:与LV-GFP组和空白对照组比较,LV-CDX2-GFP组细胞增殖活力明显降低(P<0.05),G0/G1期所占比例上升(P<0.05),Bcl-2、cyclin D1和survivin mRNA和蛋白的表达降低(P<0.05),Bax mRNA和蛋白的表达上调(P<0.05),而LV-GFP组与空白对照组比较,差异无统计学意义(P>0.05)。结论:慢病毒介导的CDX2过表达抑制胃癌细胞增殖和生长,使细胞周期停滞在G0/G1期,其机制可能与CDX2过表达使胃癌细胞Bcl-2、cyclin D1、survivin表达下调和Bax表达上调有关。
目的:探索CDX2過錶達對人胃癌SGC-7901細胞增殖、生長和細胞週期的影響及其分子機製。方法:採用攜帶CDX2基因的重組慢病毒顆粒( LV-CDX2-GFP)感染SGC-7901細胞,作為實驗組( LV-CDX2-GFP組);以對照慢病毒顆粒( LV-GFP)感染SGC-7901細胞,作為陰性對照組( LV-GFP組);空白對照組常規培養,不做任何處理。分彆採用CCK-8法檢測細胞的增殖活力,流式細胞術檢測各組細胞週期的分佈,半定量逆轉錄-聚閤酶鏈反應( RT-PCR)和Western blotting 技術檢測細胞中CDX2、Bax、Bcl-2、cyclin D1和survivin mRNA和蛋白的錶達。結果:與LV-GFP組和空白對照組比較,LV-CDX2-GFP組細胞增殖活力明顯降低(P<0.05),G0/G1期所佔比例上升(P<0.05),Bcl-2、cyclin D1和survivin mRNA和蛋白的錶達降低(P<0.05),Bax mRNA和蛋白的錶達上調(P<0.05),而LV-GFP組與空白對照組比較,差異無統計學意義(P>0.05)。結論:慢病毒介導的CDX2過錶達抑製胃癌細胞增殖和生長,使細胞週期停滯在G0/G1期,其機製可能與CDX2過錶達使胃癌細胞Bcl-2、cyclin D1、survivin錶達下調和Bax錶達上調有關。
목적:탐색CDX2과표체대인위암SGC-7901세포증식、생장화세포주기적영향급기분자궤제。방법:채용휴대CDX2기인적중조만병독과립( LV-CDX2-GFP)감염SGC-7901세포,작위실험조( LV-CDX2-GFP조);이대조만병독과립( LV-GFP)감염SGC-7901세포,작위음성대조조( LV-GFP조);공백대조조상규배양,불주임하처리。분별채용CCK-8법검측세포적증식활력,류식세포술검측각조세포주기적분포,반정량역전록-취합매련반응( RT-PCR)화Western blotting 기술검측세포중CDX2、Bax、Bcl-2、cyclin D1화survivin mRNA화단백적표체。결과:여LV-GFP조화공백대조조비교,LV-CDX2-GFP조세포증식활력명현강저(P<0.05),G0/G1기소점비례상승(P<0.05),Bcl-2、cyclin D1화survivin mRNA화단백적표체강저(P<0.05),Bax mRNA화단백적표체상조(P<0.05),이LV-GFP조여공백대조조비교,차이무통계학의의(P>0.05)。결론:만병독개도적CDX2과표체억제위암세포증식화생장,사세포주기정체재G0/G1기,기궤제가능여CDX2과표체사위암세포Bcl-2、cyclin D1、survivin표체하조화Bax표체상조유관。
AIM:To study the effect and the molecular mechanism of CDX 2 over-expression on the prolifera-tion, growth and cell cycle of human gastric cancer cell line SGC-7901.METHODS:The SGC-7901 cells in LV-CDX2-GFP group were transfected with the recombinant lentivirus vector LV-CDX2-GFP, the cells in LV-GFP group were trans-fected with the negative control lentiviral vector for the negative control , and the cells in blank control group were without any treatment.The cell proliferation was detected by CCK-8 assay.The cell cycle distribution was analyzed by flow cytome-try.The expression of CDX2, Bax, Bcl-2, cyclin D1 and survivin was determined by semi-quantitative RT-PCR and Wes-tern blotting .RESULTS:Compared with LV-GFP group and blank control group , the proliferation activity of the SGC-7901 cells was significantly lower (P<0.05), the G0/G1 phase proportion increased (P<0.05), the mRNA and protein levels of Bcl-2, cyclin D1 and survivin were reduced (P<0.05), and the mRNA and protein levels of Bax were up-regula-ted (P<0.05) in LV-CDX2-GFP group.No statistically significant difference of the above indexes was observed (P>0.05) between LV-GFP group and blank control group .CONCLUSION:Over-expression of CDX2 mediated by lentivirus inhibits the proliferation and growth of human gastric cancer SGC-7901 cells and arrestes the cell cycle at G 0/G1 phase, which may be related to down-regulation of Bcl-2, cyclin D1 and survivin and up-regulation of Bax .