中国病理生理杂志
中國病理生理雜誌
중국병리생리잡지
CHINESE JOURNAL OF PATHOPHYSIOLOGY
2015年
4期
620-624
,共5页
DEC1基因%食管癌%ECA109细胞%细胞增殖%细胞侵袭
DEC1基因%食管癌%ECA109細胞%細胞增殖%細胞侵襲
DEC1기인%식관암%ECA109세포%세포증식%세포침습
DEC1 gene%Esophageal cancer%ECA109 cells%Cell proliferation%Cell invasion
目的:探讨DEC1基因过表达对人食管癌ECA109细胞增殖和侵袭能力的影响及可能机制。方法:将质粒pcDNA3.1(-)/DEC1(DEC1组)和pcDNA3.1(-)(vector组)利用脂质体分别转染至人食管癌ECA109细胞中,通过real-time PCR检测转染48 h后的细胞内DEC1 mRNA表达,Western blot分别检测转染72 h后细胞内DEC1、基质金属蛋白酶9( MMP9)及细胞周期蛋白cyclin D1的蛋白表达;采用CCK-8实验、平板集落实验及Tran-swell实验分别检测DEC1过表达对细胞的增殖和侵袭能力的影响。结果:与vector组相比,DEC1组中DEC1的表达明显增高(P<0.01);cyclin D1和MMP9的表达明显降低(P<0.05);细胞增殖与侵袭能力明显受到抑制(P<0.01)。结论:过表达DEC1可明显抑制ECA109细胞的增殖和侵袭能力,DEC1可能通过影响MMP9和cyclin D1参与其中。
目的:探討DEC1基因過錶達對人食管癌ECA109細胞增殖和侵襲能力的影響及可能機製。方法:將質粒pcDNA3.1(-)/DEC1(DEC1組)和pcDNA3.1(-)(vector組)利用脂質體分彆轉染至人食管癌ECA109細胞中,通過real-time PCR檢測轉染48 h後的細胞內DEC1 mRNA錶達,Western blot分彆檢測轉染72 h後細胞內DEC1、基質金屬蛋白酶9( MMP9)及細胞週期蛋白cyclin D1的蛋白錶達;採用CCK-8實驗、平闆集落實驗及Tran-swell實驗分彆檢測DEC1過錶達對細胞的增殖和侵襲能力的影響。結果:與vector組相比,DEC1組中DEC1的錶達明顯增高(P<0.01);cyclin D1和MMP9的錶達明顯降低(P<0.05);細胞增殖與侵襲能力明顯受到抑製(P<0.01)。結論:過錶達DEC1可明顯抑製ECA109細胞的增殖和侵襲能力,DEC1可能通過影響MMP9和cyclin D1參與其中。
목적:탐토DEC1기인과표체대인식관암ECA109세포증식화침습능력적영향급가능궤제。방법:장질립pcDNA3.1(-)/DEC1(DEC1조)화pcDNA3.1(-)(vector조)이용지질체분별전염지인식관암ECA109세포중,통과real-time PCR검측전염48 h후적세포내DEC1 mRNA표체,Western blot분별검측전염72 h후세포내DEC1、기질금속단백매9( MMP9)급세포주기단백cyclin D1적단백표체;채용CCK-8실험、평판집락실험급Tran-swell실험분별검측DEC1과표체대세포적증식화침습능력적영향。결과:여vector조상비,DEC1조중DEC1적표체명현증고(P<0.01);cyclin D1화MMP9적표체명현강저(P<0.05);세포증식여침습능력명현수도억제(P<0.01)。결론:과표체DEC1가명현억제ECA109세포적증식화침습능력,DEC1가능통과영향MMP9화cyclin D1삼여기중。
[ ABSTRACT] AIM:To investigate the effect of DEC1 gene over-expression on the proliferation and invasion abili-ties of human esophageal cancer ECA109 cells.METHODS: ECA109 cells were transfected with plasmid pcDNA3.1 (-)/DEC1 (DEC1 group) or pcDNA3.1 (-) (vector group).The mRNA and protein levels of DEC1, cyclin D1 and MMP-9 were evaluated by real-time PCR and Western blot, respectively.The effects of DEC1 over-expression on the prolif-eration and invasion abilities of the ECA109 cells were evaluated by CCK-8 assay, colony formation assay and Transwell test respectively.RESULTS:The DEC1 expression level in ECA109 cells in DEC1 group was significantly higher than that in vector group (P<0.01), but the levels of MMP9 and cyclin D1 expression were opposite (P<0.01).However, both the proliferation and invasion abilities of ECA109 cells in DEC1 groups decreased significantly as compared with those in vector group (P<0.05).CONCLUSION:The over-expression of DEC1 significantly inhibits the proliferation and invasion of ECA109 cells, which may be involved in the expression of cyclin D1 and MMP9.