中华泌尿外科杂志
中華泌尿外科雜誌
중화비뇨외과잡지
CHINESE JOURNAL OF UROLOGY
2012年
12期
943-946
,共4页
萧云备%李晶%张晓威%刘振华%郁卫东%乔正国%牛屹东%徐涛%王晓峰
蕭雲備%李晶%張曉威%劉振華%鬱衛東%喬正國%牛屹東%徐濤%王曉峰
소운비%리정%장효위%류진화%욱위동%교정국%우흘동%서도%왕효봉
前列腺肿瘤%趋化素样因子超家族成员5%PI3K-AKT信号通路%动物实验
前列腺腫瘤%趨化素樣因子超傢族成員5%PI3K-AKT信號通路%動物實驗
전렬선종류%추화소양인자초가족성원5%PI3K-AKT신호통로%동물실험
Prostatic neoplasms%CKLF-like Marvel transmembrane domain containing 5%Pi3kakt%Animal experimentation
目的 探讨趋化素样因子超家族成员5(CMTM5)对前列腺癌细胞的作用及机制.方法 利用划痕实验观察CMTM5对前列腺癌、DU145细胞迁移的影响；蛋白质印迹法检测PI3 K-AKT信号通路相关蛋白的表达；建立18只裸鼠皮下前列腺癌移植瘤模型,实验组肿瘤局部注射CMTM5腺病毒,检测CMTM5过表达对裸鼠前列腺肿瘤生长的影响,应用免疫组织化学方法检测裸鼠肿瘤组织中Ki-67的表达. 结果 过表达CMTM5抑制前列腺癌DU145细胞迁移,减少了PI3K-AKT信号通路中的关键分子pAKT 、NF-kB等蛋白的表达.裸鼠体内实验结果显示,CMTM5组肿瘤体积及质量分别为(573.39±175.24)mm3及(0.55±0.11)g,对照组分别为(1482.50±327.86) mm3及(1.31±0.29)g,2组比较差异均有统计学意义(P＜0.05).CMTM5组肿瘤组织Ki-67表达明显低于对照组. 结论 过表达CMTM5抑制前列腺肿瘤的增殖及迁移能力,其机制与PI3K-AKT信号通路有关.
目的 探討趨化素樣因子超傢族成員5(CMTM5)對前列腺癌細胞的作用及機製.方法 利用劃痕實驗觀察CMTM5對前列腺癌、DU145細胞遷移的影響；蛋白質印跡法檢測PI3 K-AKT信號通路相關蛋白的錶達；建立18隻裸鼠皮下前列腺癌移植瘤模型,實驗組腫瘤跼部註射CMTM5腺病毒,檢測CMTM5過錶達對裸鼠前列腺腫瘤生長的影響,應用免疫組織化學方法檢測裸鼠腫瘤組織中Ki-67的錶達. 結果 過錶達CMTM5抑製前列腺癌DU145細胞遷移,減少瞭PI3K-AKT信號通路中的關鍵分子pAKT 、NF-kB等蛋白的錶達.裸鼠體內實驗結果顯示,CMTM5組腫瘤體積及質量分彆為(573.39±175.24)mm3及(0.55±0.11)g,對照組分彆為(1482.50±327.86) mm3及(1.31±0.29)g,2組比較差異均有統計學意義(P＜0.05).CMTM5組腫瘤組織Ki-67錶達明顯低于對照組. 結論 過錶達CMTM5抑製前列腺腫瘤的增殖及遷移能力,其機製與PI3K-AKT信號通路有關.
목적 탐토추화소양인자초가족성원5(CMTM5)대전렬선암세포적작용급궤제.방법 이용화흔실험관찰CMTM5대전렬선암、DU145세포천이적영향；단백질인적법검측PI3 K-AKT신호통로상관단백적표체；건립18지라서피하전렬선암이식류모형,실험조종류국부주사CMTM5선병독,검측CMTM5과표체대라서전렬선종류생장적영향,응용면역조직화학방법검측라서종류조직중Ki-67적표체. 결과 과표체CMTM5억제전렬선암DU145세포천이,감소료PI3K-AKT신호통로중적관건분자pAKT 、NF-kB등단백적표체.라서체내실험결과현시,CMTM5조종류체적급질량분별위(573.39±175.24)mm3급(0.55±0.11)g,대조조분별위(1482.50±327.86) mm3급(1.31±0.29)g,2조비교차이균유통계학의의(P＜0.05).CMTM5조종류조직Ki-67표체명현저우대조조. 결론 과표체CMTM5억제전렬선종류적증식급천이능력,기궤제여PI3K-AKT신호통로유관.
Objective To study the effect and mechanism of CKLF-like Marvel transmembrane domain containing 5 (CMTMS) on prostate cancer cell proliferation,migration and invasion.Methods The inhibitory effects of CMTM5 on the migration of DU145 cells were studied in vitro by wound healing assay.The expression of the cell signal pathway PI3K-AKT protein was detected by Western blot.The inhibition of tumor growth was also studied in transplanted prostate cancer nude mice model treated with CMTM5 adenovirus.The expression of CMTM5 and ki-67 in transplanted prostate cancer tissue of the nude mice model was analyzed immunohisochemistically.Prostate tumor volume in the nude mice model and the proliferation were measured two weeksafter.injection..Results Wound healing assay showed that over-expression of CMTM5 can inhibit the migration of DU145 cells.The expression of pAKT and NF-kB was significantly decreased after the overexpression of CMTM5.The tumor volume (573.39 ± 175.24) mm3,weight (0.55 ± 0.11) g and proliferation index of prostate in CMTM5 orthotopic injection nude mice model were significantly smaller and decreased than those in the control group (1482.50 ± 327.86) mm3 and (1.31 ± 0.29) g (P ＜ 0.05).Conclusions Both in vitro and in vivo experiments demonstrate that overexpression of CMTM5 could suppress prostate cancer cell proliferation,migration and invasion.The effect may be conducted by PI3K-AKT signaling pathway.
