CAJ | 학술논문

目的观察趋化因子受体5(CCR5)对乳腺癌干细胞(CD44+CD24-/low)趋化和侵袭作用.方法应用流式细胞仪分选获得乳腺癌干细胞,逆转录-聚合酶链反应(RT-PCR)和酶联免疫吸附试验(ELISA)检测乳腺癌MCF-72个SP侧群细胞(side population)6例样本CCR5 mRNA和蛋白质,在趋化因子5(CCL5)作用下通过趋化小室法检测2个SP侧群细胞趋化活性和侵袭活性,并与CCR5的封闭进行对照研究.结果 CCL5对MCF-7肿瘤干细胞有明显趋化[乳腺癌干细胞(86.0±14.8)个/HP与CD44+CD24+(72.0±13.5)个/HP,t=7.461,P<0.05]和侵袭作用[乳腺癌干细胞(25.0±8.3)个/HP与CD44+CD24+(16.0±5.4)个/HP,t=6.665,P<0.05].结论 CCB5表达能够促进乳腺癌干细胞趋化和侵袭.
목적 관찰추화인자수체5(CCR5)대유선암간세포(CD44+CD24-/low)추화화침습작용.방법 응용류식세포의분선획득유선암간세포,역전록-취합매련반응(RT-PCR)화매련면역흡부시험(ELISA)검측유선암MCF-72개SP측군세포(side population)6례양본CCR5 mRNA화단백질,재추화인자5(CCL5)작용하통과추화소실법검측2개SP측군세포추화활성화침습활성,병여CCR5적봉폐진행대조연구.결과 CCL5대MCF-7종류간세포유명현추화[유선암간세포(86.0±14.8)개/HP여CD44+CD24+(72.0±13.5)개/HP,t=7.461,P<0.05]화침습작용[유선암간세포(25.0±8.3)개/HP여CD44+CD24+(16.0±5.4)개/HP,t=6.665,P<0.05].결론 CCB5표체능구촉진유선암간세포추화화침습.
Objective To study the chemotaxis and invasion of breast cancer stem cells facilita-ted by CC chemokine receptor-5 (CCR5). Methods Breast cancer stem cells in MCF-7 were isolate by fluorescence-activated cell sorting, RT-PCR and ELISA were used to detect the expression of CCR5 at mR-NA and protein level in six samples. The chemotaxis and invasion of two subpopulation of MCF-7 were in-duced by CCLS, and the results were compared with those which were blocked with CCR5. Results CCL5 regulate chemotaxis [CD44+CD24-/low(86.0±14.8)/HP vs CD44+ CD24+ (72.0±13.5 ), t=7.461, P<0.05] and invasion [CD44+ CD24-/low(25.0±8.3)/HP vs CD44+CD24+ (16.0±5.4) /HP,t= 6.665,P<0.05] in CD44+CD24-/low subpopulation cells obviously. Conclusion Chemotaxis and inva-sion of breast cancer stem cells can be facilitated by CCR5 expression.