中华泌尿外科杂志
中華泌尿外科雜誌
중화비뇨외과잡지
CHINESE JOURNAL OF UROLOGY
2014年
7期
543-546
,共4页
p120-连环蛋白%BIU-87细胞%增殖%侵袭%黏附
p120-連環蛋白%BIU-87細胞%增殖%侵襲%黏附
p120-련배단백%BIU-87세포%증식%침습%점부
p120-catenin%BIU-87 cell%Proliferation%Invasion%Adhesion
目的:探讨p120-连环蛋白在膀胱癌BIU-87和T24细胞株中的表达水平,分析p120-连环蛋白下调对膀胱癌BIU-87细胞增殖、侵袭和黏附能力的影响。方法2010年8月至2011年5月,采用实时定量PCR和蛋白质印迹技术检测膀胱癌BIU-87和T24细胞株中p120-连环蛋白的表达水平。将膀胱癌 BIU-87细胞分为3组:未转染组,转染p120-连环蛋白siRNA 组和转染control siRNA组,应用siRNA方法沉默BIU-87细胞中p120-连环蛋白基因表达,采用噻唑盐法和克隆形成实验检测p120-连环蛋白siRNA对BIU-87细胞生长率的影响,Transwell小室法检测BIU-87细胞侵袭能力的变化,细胞黏附人工重组基底膜实验检测BIU-87细胞黏附能力的变化。结果 p120-连环蛋白在膀胱癌BIU-87和T24细胞株中均有表达,在BIU-87细胞株中的表达水平(0.11±0.39)显著高于T24细胞株(0.48±0.17),差异有统计学意义(P<0.05)。噻唑盐法检测BIU-87细胞的增殖能力,转染p120-连环蛋白siRNA组的生长增殖率(182.7±13.4)%显著高于转染control siRNA组的(95.5±9.9)%和未转染组的100.0%,差异有统计学意义( P<0.05)。转染p120-连环蛋白siRNA组BIU-87细胞侵袭数量[(217.5±15.9)个]明显高于转染 control siRNA 组[(105.4±10.1)个]和未转染组[(92.7±8.3)个],差异有统计学意义( P<0.05)。转染 p120-连环蛋白 siRNA 组 BIU-87细胞的黏附能力(57.3±6.4)%明显低于转染control siRNA组(98.1±11.0)%和未转染组100.0%,差异有统计学意义( P<0.05)。结论 p120-连环蛋白在恶性度低的膀胱癌细胞中表达水平高,其表达下调可促进膀胱癌细胞的增殖和侵袭,抑制膀胱癌细胞的黏附。
目的:探討p120-連環蛋白在膀胱癌BIU-87和T24細胞株中的錶達水平,分析p120-連環蛋白下調對膀胱癌BIU-87細胞增殖、侵襲和黏附能力的影響。方法2010年8月至2011年5月,採用實時定量PCR和蛋白質印跡技術檢測膀胱癌BIU-87和T24細胞株中p120-連環蛋白的錶達水平。將膀胱癌 BIU-87細胞分為3組:未轉染組,轉染p120-連環蛋白siRNA 組和轉染control siRNA組,應用siRNA方法沉默BIU-87細胞中p120-連環蛋白基因錶達,採用噻唑鹽法和剋隆形成實驗檢測p120-連環蛋白siRNA對BIU-87細胞生長率的影響,Transwell小室法檢測BIU-87細胞侵襲能力的變化,細胞黏附人工重組基底膜實驗檢測BIU-87細胞黏附能力的變化。結果 p120-連環蛋白在膀胱癌BIU-87和T24細胞株中均有錶達,在BIU-87細胞株中的錶達水平(0.11±0.39)顯著高于T24細胞株(0.48±0.17),差異有統計學意義(P<0.05)。噻唑鹽法檢測BIU-87細胞的增殖能力,轉染p120-連環蛋白siRNA組的生長增殖率(182.7±13.4)%顯著高于轉染control siRNA組的(95.5±9.9)%和未轉染組的100.0%,差異有統計學意義( P<0.05)。轉染p120-連環蛋白siRNA組BIU-87細胞侵襲數量[(217.5±15.9)箇]明顯高于轉染 control siRNA 組[(105.4±10.1)箇]和未轉染組[(92.7±8.3)箇],差異有統計學意義( P<0.05)。轉染 p120-連環蛋白 siRNA 組 BIU-87細胞的黏附能力(57.3±6.4)%明顯低于轉染control siRNA組(98.1±11.0)%和未轉染組100.0%,差異有統計學意義( P<0.05)。結論 p120-連環蛋白在噁性度低的膀胱癌細胞中錶達水平高,其錶達下調可促進膀胱癌細胞的增殖和侵襲,抑製膀胱癌細胞的黏附。
목적:탐토p120-련배단백재방광암BIU-87화T24세포주중적표체수평,분석p120-련배단백하조대방광암BIU-87세포증식、침습화점부능력적영향。방법2010년8월지2011년5월,채용실시정량PCR화단백질인적기술검측방광암BIU-87화T24세포주중p120-련배단백적표체수평。장방광암 BIU-87세포분위3조:미전염조,전염p120-련배단백siRNA 조화전염control siRNA조,응용siRNA방법침묵BIU-87세포중p120-련배단백기인표체,채용새서염법화극륭형성실험검측p120-련배단백siRNA대BIU-87세포생장솔적영향,Transwell소실법검측BIU-87세포침습능력적변화,세포점부인공중조기저막실험검측BIU-87세포점부능력적변화。결과 p120-련배단백재방광암BIU-87화T24세포주중균유표체,재BIU-87세포주중적표체수평(0.11±0.39)현저고우T24세포주(0.48±0.17),차이유통계학의의(P<0.05)。새서염법검측BIU-87세포적증식능력,전염p120-련배단백siRNA조적생장증식솔(182.7±13.4)%현저고우전염control siRNA조적(95.5±9.9)%화미전염조적100.0%,차이유통계학의의( P<0.05)。전염p120-련배단백siRNA조BIU-87세포침습수량[(217.5±15.9)개]명현고우전염 control siRNA 조[(105.4±10.1)개]화미전염조[(92.7±8.3)개],차이유통계학의의( P<0.05)。전염 p120-련배단백 siRNA 조 BIU-87세포적점부능력(57.3±6.4)%명현저우전염control siRNA조(98.1±11.0)%화미전염조100.0%,차이유통계학의의( P<0.05)。결론 p120-련배단백재악성도저적방광암세포중표체수평고,기표체하조가촉진방광암세포적증식화침습,억제방광암세포적점부。
Objective To investigate the expression of p 120-catenin in human bladder cell line BIU-87 and T24.And to explore the effect of down-regulation of p120-catenin on proliferation, invasion and adhesion of BIU-87 cell line. Methods The study was from Aug .2010 to May.2011.Real-time RT-PCR and Western blot were used to examine the expression of p 120-catenin in human bladder cell line BIU-87 and T24.There were three study groups:non-transfected group , the group transfected with p 120-catenin siRNA and the group transfected with control siRNA .p120-catenin siRNA was used to decrease the expression of p120-catenin.MTT assay and colony formation assay were used to study the BIU-87 cell growth and cell pro-liferation.The invasion of BIU-87 cells was measured by Transwell chamber assay .Cell adhesion artificial re-constituted basement membrane assay was used to examine the change of BIU-87 cell adhesion capacity . Results In both BIU-87 and T24 cells there were the expressions of p 120-catenin.But the expression in BIU-87 cells (0.11±0.39) was more than that in T24 cells (0.48±0.17).The decreased of p120-catenin ex-pression could enhance the proliferation (182.7±13.4%) and the invasiveness (217.5±15.9) and decrease the adhesion capacity (57.3±6.4%) of BIU-87 cells. Conclusions There is higher expression level of p120-catenin in lower-grade malignant bladder cancer cells .The down-regulation of p120-catenin promotes the bladder cancer proliferation and invasiveness of bladder carcinoma cells , and inhibited the bladder canc-er cell adhesion .