中国医药
中國醫藥
중국의약
CHINA MEDICINE
2013年
1期
86-88
,共3页
郭满盈%张茵%罗雪平%陈扬%王栋
郭滿盈%張茵%囉雪平%陳颺%王棟
곽만영%장인%라설평%진양%왕동
乳腺肿瘤%乳腺细胞,培养的%受体,趋化因子
乳腺腫瘤%乳腺細胞,培養的%受體,趨化因子
유선종류%유선세포,배양적%수체,추화인자
Breast neoplasms%Tumor cells,cultured%Receptors,chemokine
目的 探讨趋化因子受体5(CCR5)及其配体(RANTES)对乳腺癌细胞趋化活性和侵袭活性的促进作用.方法 用反转录聚合酶链反应、免疫组织化学法测定乳腺癌细胞株MCF-7的CCR5 mRNA及蛋白水平,RANTES的作用下,以无血清RPMI 1640培养液作为阴性对照组,含乳腺癌细胞的无血清RPMI1640培养液为对照组,加有CCR5mAb的乳腺癌细胞无血清RPMI 1640为实验组,通过趋化小室法检测MCF-7细胞的趋化活性和侵袭活性,并与CCR5的封闭进行对照研究.结果 迁移至多聚碳酸酯膜背面的乳腺癌细胞数明显多于相应的阴性对照组,实验组和对照组迁移至多聚碳酸酯膜背面的细胞分别为(73.0±9.8)、(7.6±1.5)个/HP,差异有统计学意义(=11.85,P<0.01);穿透Matrigel基质胶到达多聚碳酸酯膜背面的乳腺癌细胞数明显多于相应的阴性对照组,实验组和对照组迁移至多聚碳酸酯膜背面的细胞分别为(19.7±4.0)、(2.3±0.6)个/HP,差异有统计学意义(=7.37,P<0.01).乳腺癌细胞株MCF-7有CCR5mRNA及蛋白质的表达,其配体RANTES对MCF-7细胞有明显的趋化活性和侵袭活性,CCR5的封闭也能抑制MCF-7细胞的这种趋化活性和侵袭活性.结论 乳腺癌细胞株MCF-7有CCR5的表达,且其表达能够促进MCF-7细胞的趋化和侵袭.
目的 探討趨化因子受體5(CCR5)及其配體(RANTES)對乳腺癌細胞趨化活性和侵襲活性的促進作用.方法 用反轉錄聚閤酶鏈反應、免疫組織化學法測定乳腺癌細胞株MCF-7的CCR5 mRNA及蛋白水平,RANTES的作用下,以無血清RPMI 1640培養液作為陰性對照組,含乳腺癌細胞的無血清RPMI1640培養液為對照組,加有CCR5mAb的乳腺癌細胞無血清RPMI 1640為實驗組,通過趨化小室法檢測MCF-7細胞的趨化活性和侵襲活性,併與CCR5的封閉進行對照研究.結果 遷移至多聚碳痠酯膜揹麵的乳腺癌細胞數明顯多于相應的陰性對照組,實驗組和對照組遷移至多聚碳痠酯膜揹麵的細胞分彆為(73.0±9.8)、(7.6±1.5)箇/HP,差異有統計學意義(=11.85,P<0.01);穿透Matrigel基質膠到達多聚碳痠酯膜揹麵的乳腺癌細胞數明顯多于相應的陰性對照組,實驗組和對照組遷移至多聚碳痠酯膜揹麵的細胞分彆為(19.7±4.0)、(2.3±0.6)箇/HP,差異有統計學意義(=7.37,P<0.01).乳腺癌細胞株MCF-7有CCR5mRNA及蛋白質的錶達,其配體RANTES對MCF-7細胞有明顯的趨化活性和侵襲活性,CCR5的封閉也能抑製MCF-7細胞的這種趨化活性和侵襲活性.結論 乳腺癌細胞株MCF-7有CCR5的錶達,且其錶達能夠促進MCF-7細胞的趨化和侵襲.
목적 탐토추화인자수체5(CCR5)급기배체(RANTES)대유선암세포추화활성화침습활성적촉진작용.방법 용반전록취합매련반응、면역조직화학법측정유선암세포주MCF-7적CCR5 mRNA급단백수평,RANTES적작용하,이무혈청RPMI 1640배양액작위음성대조조,함유선암세포적무혈청RPMI1640배양액위대조조,가유CCR5mAb적유선암세포무혈청RPMI 1640위실험조,통과추화소실법검측MCF-7세포적추화활성화침습활성,병여CCR5적봉폐진행대조연구.결과 천이지다취탄산지막배면적유선암세포수명현다우상응적음성대조조,실험조화대조조천이지다취탄산지막배면적세포분별위(73.0±9.8)、(7.6±1.5)개/HP,차이유통계학의의(=11.85,P<0.01);천투Matrigel기질효도체다취탄산지막배면적유선암세포수명현다우상응적음성대조조,실험조화대조조천이지다취탄산지막배면적세포분별위(19.7±4.0)、(2.3±0.6)개/HP,차이유통계학의의(=7.37,P<0.01).유선암세포주MCF-7유CCR5mRNA급단백질적표체,기배체RANTES대MCF-7세포유명현적추화활성화침습활성,CCR5적봉폐야능억제MCF-7세포적저충추화활성화침습활성.결론 유선암세포주MCF-7유CCR5적표체,차기표체능구촉진MCF-7세포적추화화침습.
Objective To study the chemotaxis and invasion of breast cancer cells facilitated by chemokine receptor 5 (CCR5) and its ligand.Methods Reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemical staining were used todetect CCR5 mRNA and protein expression in breast cancer cells MCF-7 ;the chemotaxis and invasion of MCF-7 were performed by using Boyden chambers in presence of activation normal T-cell and secreted(RANTES) which is a ligand of CCR5.Results The number of cells migrating to the opposite side of polycarbonate membrane was significantly higher than that of negative control group,which was (73.0 ±9.8) and(7.6 ± 1.5)/HP respectively (t =11.85,P < 0.01).The number of cells penetrating Matrigel gel and migrating to the opposite side of polycarbonate membrane was significantly higher than that of negative control group [(19.7 ± 4.0) and (2.3 ± 0.6)/HP respectively (t =7.37,P < 0.01)].Breast cancer cells MCF-7 expressed CCR5 mRNA and protein,and RANTES-mediated chemotaxis and invasion could be checked in the breast cancer cells.Both chemotaxis and invasion could be blocked by neutralizing anti-CCR5 antibody.Conclusions Breast cancer cells MCF-7 expressed CCR5 and chemotaxis and invasion of MCF-7 can be facilitated by CCR5 expression.