中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
CHINESE JOURNAL OF EXPERIMENTAL SURGERY
2014年
11期
2411-2413
,共3页
李海杰%杨熹%葛宗庆%兰静芩%李国东%付寅佳%穆磊%江旭林%胡俊波
李海傑%楊熹%葛宗慶%蘭靜芩%李國東%付寅佳%穆磊%江旭林%鬍俊波
리해걸%양희%갈종경%란정금%리국동%부인가%목뢰%강욱림%호준파
组蛋白赖氨酸残基去甲基化酶4B%乳腺癌%上皮-间充质转化%迁移%侵袭
組蛋白賴氨痠殘基去甲基化酶4B%乳腺癌%上皮-間充質轉化%遷移%侵襲
조단백뢰안산잔기거갑기화매4B%유선암%상피-간충질전화%천이%침습
Lysine (K)-specific demethylase 4B%Breast cancer%Epithelial-mesenchymal transition%Migration%Invasion
目的 构建组蛋白赖氨酸残基去甲基化酶4B(KDM4B)过表达乳腺癌细胞株MCF-7,观察KDM4B对MCF-7侵袭迁移能力的影响,并探索其机制.方法 利用KDM4B慢病毒感染乳腺癌细胞株MCF-7,筛选KDM4B过表达稳定细胞株,Western blot法检测MCF-7细胞中KDM4B基因蛋白表达;迁移实验、侵袭实验观察过表达KDM4B对乳腺癌MCF-7细胞迁移和侵袭能力的影响;Western blot法检测细胞上皮-间充质转化相关蛋白E-钙黏蛋白(E-cadherin)、波形蛋白(Vimentin)表达.结果 Western blot法验证过表达KDM4B的乳腺癌细胞株MCF-7构建成功;迁移实验中过表达KDM4B细胞穿膜数目[(94±8)个]较对照组[(36±6)个]明显增多,侵袭实验中过表达KDM4B细胞穿膜数目[(18±2)个]较对照组[(5±1)个]明显增多,差异均有统计学意义(P＜0.01);过表达KDM4B细胞中E-cadherin表达量较对照组明显降低,Vimentin表达量较对照组明显增高.结论 过表达KDM4B基因可促进乳腺癌细胞株MCF-7上皮-间充质转化过程,并提高细胞迁移、侵袭能力.
目的 構建組蛋白賴氨痠殘基去甲基化酶4B(KDM4B)過錶達乳腺癌細胞株MCF-7,觀察KDM4B對MCF-7侵襲遷移能力的影響,併探索其機製.方法 利用KDM4B慢病毒感染乳腺癌細胞株MCF-7,篩選KDM4B過錶達穩定細胞株,Western blot法檢測MCF-7細胞中KDM4B基因蛋白錶達;遷移實驗、侵襲實驗觀察過錶達KDM4B對乳腺癌MCF-7細胞遷移和侵襲能力的影響;Western blot法檢測細胞上皮-間充質轉化相關蛋白E-鈣黏蛋白(E-cadherin)、波形蛋白(Vimentin)錶達.結果 Western blot法驗證過錶達KDM4B的乳腺癌細胞株MCF-7構建成功;遷移實驗中過錶達KDM4B細胞穿膜數目[(94±8)箇]較對照組[(36±6)箇]明顯增多,侵襲實驗中過錶達KDM4B細胞穿膜數目[(18±2)箇]較對照組[(5±1)箇]明顯增多,差異均有統計學意義(P＜0.01);過錶達KDM4B細胞中E-cadherin錶達量較對照組明顯降低,Vimentin錶達量較對照組明顯增高.結論 過錶達KDM4B基因可促進乳腺癌細胞株MCF-7上皮-間充質轉化過程,併提高細胞遷移、侵襲能力.
목적 구건조단백뢰안산잔기거갑기화매4B(KDM4B)과표체유선암세포주MCF-7,관찰KDM4B대MCF-7침습천이능력적영향,병탐색기궤제.방법 이용KDM4B만병독감염유선암세포주MCF-7,사선KDM4B과표체은정세포주,Western blot법검측MCF-7세포중KDM4B기인단백표체;천이실험、침습실험관찰과표체KDM4B대유선암MCF-7세포천이화침습능력적영향;Western blot법검측세포상피-간충질전화상관단백E-개점단백(E-cadherin)、파형단백(Vimentin)표체.결과 Western blot법험증과표체KDM4B적유선암세포주MCF-7구건성공;천이실험중과표체KDM4B세포천막수목[(94±8)개]교대조조[(36±6)개]명현증다,침습실험중과표체KDM4B세포천막수목[(18±2)개]교대조조[(5±1)개]명현증다,차이균유통계학의의(P＜0.01);과표체KDM4B세포중E-cadherin표체량교대조조명현강저,Vimentin표체량교대조조명현증고.결론 과표체KDM4B기인가촉진유선암세포주MCF-7상피-간충질전화과정,병제고세포천이、침습능력.
Objective To construct lentivirus-induced lysine (K)-specific demethylase 4B (KDM4B) overexpression breast cancer cell MCF-7 and observe the effect of KDM4B on the invasion and migration ability of breast cancer cell MCF-7,and explore the underlying mechanism.Methods Lentivirus-induced KDM4B over-expression was used for in vitro function analyses in breast cancer cell line MCF-7,including migration and invasion assay,and Western blotting assay.Results Compared to the control,the expression of KDM4B was significantly increased in the experimental group,while the expression of E-cadherin was significantly decreased and Vimentin was significantly increased.In the migration assay,the number of penetrating the membrane was markedly increased in the experimental group as campared with the control (94 ± 8 vs.36± 6).The same phenomenon was also found in the invasion assay (18 ± 2 vs.5 ± 1).Conclusion Up-regulation of KDM4B could promote the process of epithelial-mesenchymal transition,migration and invasion of breast cancer cell line MCF-7.
