中华医学杂志
中華醫學雜誌
중화의학잡지
National Medical Journal of China
2014年
34期
2704-2707
,共4页
宋佳佳%卢永宁%张进%黄翼然
宋佳佳%盧永寧%張進%黃翼然
송가가%로영저%장진%황익연
癌,肾细胞%成纤维细胞%肿瘤微环境%耐药
癌,腎細胞%成纖維細胞%腫瘤微環境%耐藥
암,신세포%성섬유세포%종류미배경%내약
Carcinoma,renal cell%Normal human renal fibroblast%Tumor microenvironment%Drug resistance
目的 观察肾癌细胞株786-O、Caki-1与正常人肾成纤维细胞(NHRF)相互作用后,肾癌细胞对依维莫司敏感性的变化.方法 建立肾癌细胞与成纤维细胞共培养体系,观察共培养后786-O、Caki-1的增殖及迁移能力[用吸光度(A)值表示]变化以及肾癌细胞对依维莫司敏感性的改变.结果 共培养后,786-O组肾癌细胞细胞增殖能力较对照组A值显著增加22％(2.35±0.05与1.93±0.15,P=0.01),Caki-1组A值较对照组显著增加约80％(2.35±0.21与1.24±0.11,P=0.001);迁移能力有所增强:786-O A值较对照组显著增加(1.34±0.12与0.86±0.04,P=0.03),Caki-1 A值较对照组显著增加(1.53 ±0.11与0.98 ±0.11,P=0.04).此外共培养组经依维莫司(1、5、10 μmol/L)处理后,在1μmol/L时,786-O组和对照组相比抑制率降低(24.05±5.05)％与(12.45±2.44)％,P=0.04,在5、10 μmol/L时抑制率无明显变化(P值分别为0.35、0.18);Caki-1共培养组和对照组相比,抑制率均明显降低(49.02±2.17)％与(4.96±0.50)％,P=0.02;(52.67±2.57)％与(12.36±0.29)％,P=0.03;(60.87±3.87)％与(35.10±2.45)％,P=0.024.结论 NHRF促进肾癌细胞株786-O、Caki-1的增殖及迁移;NHRF参与786-O、Caki-1对依维莫司耐药现象的发生.
目的 觀察腎癌細胞株786-O、Caki-1與正常人腎成纖維細胞(NHRF)相互作用後,腎癌細胞對依維莫司敏感性的變化.方法 建立腎癌細胞與成纖維細胞共培養體繫,觀察共培養後786-O、Caki-1的增殖及遷移能力[用吸光度(A)值錶示]變化以及腎癌細胞對依維莫司敏感性的改變.結果 共培養後,786-O組腎癌細胞細胞增殖能力較對照組A值顯著增加22％(2.35±0.05與1.93±0.15,P=0.01),Caki-1組A值較對照組顯著增加約80％(2.35±0.21與1.24±0.11,P=0.001);遷移能力有所增彊:786-O A值較對照組顯著增加(1.34±0.12與0.86±0.04,P=0.03),Caki-1 A值較對照組顯著增加(1.53 ±0.11與0.98 ±0.11,P=0.04).此外共培養組經依維莫司(1、5、10 μmol/L)處理後,在1μmol/L時,786-O組和對照組相比抑製率降低(24.05±5.05)％與(12.45±2.44)％,P=0.04,在5、10 μmol/L時抑製率無明顯變化(P值分彆為0.35、0.18);Caki-1共培養組和對照組相比,抑製率均明顯降低(49.02±2.17)％與(4.96±0.50)％,P=0.02;(52.67±2.57)％與(12.36±0.29)％,P=0.03;(60.87±3.87)％與(35.10±2.45)％,P=0.024.結論 NHRF促進腎癌細胞株786-O、Caki-1的增殖及遷移;NHRF參與786-O、Caki-1對依維莫司耐藥現象的髮生.
목적 관찰신암세포주786-O、Caki-1여정상인신성섬유세포(NHRF)상호작용후,신암세포대의유막사민감성적변화.방법 건립신암세포여성섬유세포공배양체계,관찰공배양후786-O、Caki-1적증식급천이능력[용흡광도(A)치표시]변화이급신암세포대의유막사민감성적개변.결과 공배양후,786-O조신암세포세포증식능력교대조조A치현저증가22％(2.35±0.05여1.93±0.15,P=0.01),Caki-1조A치교대조조현저증가약80％(2.35±0.21여1.24±0.11,P=0.001);천이능력유소증강:786-O A치교대조조현저증가(1.34±0.12여0.86±0.04,P=0.03),Caki-1 A치교대조조현저증가(1.53 ±0.11여0.98 ±0.11,P=0.04).차외공배양조경의유막사(1、5、10 μmol/L)처리후,재1μmol/L시,786-O조화대조조상비억제솔강저(24.05±5.05)％여(12.45±2.44)％,P=0.04,재5、10 μmol/L시억제솔무명현변화(P치분별위0.35、0.18);Caki-1공배양조화대조조상비,억제솔균명현강저(49.02±2.17)％여(4.96±0.50)％,P=0.02;(52.67±2.57)％여(12.36±0.29)％,P=0.03;(60.87±3.87)％여(35.10±2.45)％,P=0.024.결론 NHRF촉진신암세포주786-O、Caki-1적증식급천이;NHRF삼여786-O、Caki-1대의유막사내약현상적발생.
Objective To observe the effects of normal human renal fibroblast (NHRF) on renal cell carcinoma cell lines.Methods Renal cell carcinoma (RCC) cell lines 786-O and Caki-1 were cocultured with NHRF for assessing the proliferation and migratory capacities of renal cell carcinoma cell lines and the sensitivity to everolimus.Results Co-culturing with NHRF substantially increased the proliferation capacity of both RCC cell lines (786-O:2.35 ± 0.05 vs1.93 ± 0.15,P =0.01 ; Caki-1:2.35 ± 0.21 vs 1.24 ± 0.11,P =0.001).Similarly the migratory capacities of both cell lines became significantly enhanced after co-culturing (786-O:1.53 ± 0.11 vs 0.98 ± 0.11,P =0.04 ; Caki-1:1.53 ± 0.11 vs 0.98 ± 0.11,P =0.04) compared with untreated control.Furthermore,the sensitivities of both cell lines to everolimus (1,5,10 μmol/L) dramatically decreased in those pre-co-cultured with NHRF (786-O:P value 0.04,0.35,0.18) ; Caki-1:P value 0.02,0.03,0.024).Conclusion NHRF promotes the proliferation and migration capacities of 786-O and Caki-1.And it may be involved in the resistance of RCC to everolimus.
