中华泌尿外科杂志
中華泌尿外科雜誌
중화비뇨외과잡지
CHINESE JOURNAL OF UROLOGY
2012年
4期
250-253
,共4页
牛志宏%刘帅%毕东滨%刘征%刘晓雯%袁晓东%吕家驹
牛誌宏%劉帥%畢東濱%劉徵%劉曉雯%袁曉東%呂傢駒
우지굉%류수%필동빈%류정%류효문%원효동%려가구
肾肿瘤%肾母细胞瘤过表达%增殖%黏附
腎腫瘤%腎母細胞瘤過錶達%增殖%黏附
신종류%신모세포류과표체%증식%점부
Kidney neoplasms%Nephroblastoma overexpressed%Proliferation%Adhesion
目的 探讨肾母细胞瘤过表达( nephroblastoma overexpressed,NOV)基因对肾癌细胞增殖、黏附、侵袭和迁移能力的影响. 方法 构建NOV蛋白表达真核细胞重组表达质粒pEGFP-C1-NOV,转染人肾癌细胞株786-O.通过计数细胞绘制生长曲线、水溶性四氮唑法(WST-1)检测细胞生长抑制率,通过细胞黏附实验、侵袭实验和细胞迁移实验,比较转染pEGFP-C1 -NOV组(实验组)与转染空载体组(空载组)及未转染组(空白组)的细胞增殖、黏附、侵袭和迁移能力的差异. 结果 与空白组比较,实验组48、72 h抑制率分别为29.14%、32.46%,空载组分别为9.25%和- 8.16%,实验组与空白组比较差异有统计学意义(P<0.05),空载组与空白组相比差异无统计学意义(P>0.05).与层粘连蛋白黏附,实验组A值为0.26±0.03,高于空白组(0.15±0.01)和空载组(0.14 ±0.02),差异有统计学意义(P<0.05);与人纤维连接蛋白黏附,实验组A值为0.28±0.04,高于空白组(0.124±0.095)和空载组(0.128±0.082),差异有统计学意义(P<0.05).实验组穿越Matrigel基质胶的细胞数为240.25±23.12,显著高于空白组(56.16 ±6.25)和空载组(50.28 ±7.13),差异有统计学意义(P<0.05);实验组迁移通过聚碳酸酯微孔滤膜的细胞数为267.25±20.94,显著高于空白组(66.10 ±5.68)和空载组(56.28 ±4.11),差异有统计学意义(P<0.05). 结论 NOV可抑制肾癌细胞的增殖,促进肾癌细胞786-O的黏附、侵袭和迁移.
目的 探討腎母細胞瘤過錶達( nephroblastoma overexpressed,NOV)基因對腎癌細胞增殖、黏附、侵襲和遷移能力的影響. 方法 構建NOV蛋白錶達真覈細胞重組錶達質粒pEGFP-C1-NOV,轉染人腎癌細胞株786-O.通過計數細胞繪製生長麯線、水溶性四氮唑法(WST-1)檢測細胞生長抑製率,通過細胞黏附實驗、侵襲實驗和細胞遷移實驗,比較轉染pEGFP-C1 -NOV組(實驗組)與轉染空載體組(空載組)及未轉染組(空白組)的細胞增殖、黏附、侵襲和遷移能力的差異. 結果 與空白組比較,實驗組48、72 h抑製率分彆為29.14%、32.46%,空載組分彆為9.25%和- 8.16%,實驗組與空白組比較差異有統計學意義(P<0.05),空載組與空白組相比差異無統計學意義(P>0.05).與層粘連蛋白黏附,實驗組A值為0.26±0.03,高于空白組(0.15±0.01)和空載組(0.14 ±0.02),差異有統計學意義(P<0.05);與人纖維連接蛋白黏附,實驗組A值為0.28±0.04,高于空白組(0.124±0.095)和空載組(0.128±0.082),差異有統計學意義(P<0.05).實驗組穿越Matrigel基質膠的細胞數為240.25±23.12,顯著高于空白組(56.16 ±6.25)和空載組(50.28 ±7.13),差異有統計學意義(P<0.05);實驗組遷移通過聚碳痠酯微孔濾膜的細胞數為267.25±20.94,顯著高于空白組(66.10 ±5.68)和空載組(56.28 ±4.11),差異有統計學意義(P<0.05). 結論 NOV可抑製腎癌細胞的增殖,促進腎癌細胞786-O的黏附、侵襲和遷移.
목적 탐토신모세포류과표체( nephroblastoma overexpressed,NOV)기인대신암세포증식、점부、침습화천이능력적영향. 방법 구건NOV단백표체진핵세포중조표체질립pEGFP-C1-NOV,전염인신암세포주786-O.통과계수세포회제생장곡선、수용성사담서법(WST-1)검측세포생장억제솔,통과세포점부실험、침습실험화세포천이실험,비교전염pEGFP-C1 -NOV조(실험조)여전염공재체조(공재조)급미전염조(공백조)적세포증식、점부、침습화천이능력적차이. 결과 여공백조비교,실험조48、72 h억제솔분별위29.14%、32.46%,공재조분별위9.25%화- 8.16%,실험조여공백조비교차이유통계학의의(P<0.05),공재조여공백조상비차이무통계학의의(P>0.05).여층점련단백점부,실험조A치위0.26±0.03,고우공백조(0.15±0.01)화공재조(0.14 ±0.02),차이유통계학의의(P<0.05);여인섬유련접단백점부,실험조A치위0.28±0.04,고우공백조(0.124±0.095)화공재조(0.128±0.082),차이유통계학의의(P<0.05).실험조천월Matrigel기질효적세포수위240.25±23.12,현저고우공백조(56.16 ±6.25)화공재조(50.28 ±7.13),차이유통계학의의(P<0.05);실험조천이통과취탄산지미공려막적세포수위267.25±20.94,현저고우공백조(66.10 ±5.68)화공재조(56.28 ±4.11),차이유통계학의의(P<0.05). 결론 NOV가억제신암세포적증식,촉진신암세포786-O적점부、침습화천이.
Objective To investigate the effects of nephroblastoma overexpressed (NOV) on proliferation,adhesion,migration and invasion of remal cell curcinomai (RCC) cells. Methods We constructed a NOV expression plasmid and transfected the plasmid into RCC cell line 786-O and analyzed the effects of NOV expression on proliferation,adhesion,migration and invasion of RCC cells by growth curve assay,WST-1 assay,cell adhesion assay,matrigel invasion assay and transwell migration assay. Results The stable NOV transfected 786-O cells (786-O-NOV) showed decreased growth rate,at 48 h and 72 h,the proliferation activities of 786-O-NOV cells were inhibited by 29.14% and 32.46% the proliferation activities of empty vector cells were inhibited by 9.25% and - 8.16%,respectively,compared to 786-O cells (P <0.05); while the 786-O cells transfected with empty vector (786-O-mock) had no difference with 786-Ocells.Adhesion assay indicated significantly increased adhesion of 786-O-NOV cells to fibronectin (0.26 ±0.03) and laminin (0.28 ±0.04),compared to 786-O cells (0.15 ±0.01,0.12±0.10) and 786-O-mock cells (0.14 ±0.02,0.13 ± 0.08).Invasion assay displayed that the numbers of cells penetrated through matrigel membrane were significantly higher in 786-O-NOV cells (240.25 ± 23.12) compared to 786-O cells ( 56.16 ± 6.25 ) and 786-O-mock cells ( 50.28 ± 7.13 ).Migration assay displayed that the numbers of cells passed through polycarbonate filters were significantly higher in 786-O-NOV cells (267.25 ± 20.94) compared to 786-O cells ( 66.10 ± 5.68 ) and 786-O-mock cells ( 56.28 ± 4.11 ).Conclusion NOV exhibits anti-proliferative effects on RCC cells; however,it promotes adhesion,migration and invasion of RCC cells.