CAJ | 학술논문

目的探讨雌激素受体α(ERα)对膀胱癌细胞增殖和侵袭力的影响机制. 方法建立ERα过表达的膀胱癌细胞T24ERα模型,对照组为膀胱癌细胞株T24V空质粒组.应用四甲基偶氮唑比色法检测细胞生长情况,流式细胞技术检测细胞凋亡情况,Transwell和细胞划痕实验检测膀胱癌细胞的侵袭能力,蛋白质印迹法检测ERα调节膀胱癌细胞增殖和侵袭能力的信号通路. 结果与空质粒对照组相比,实验组在96 h和144 h细胞抑制率分别为18.85％、37.21％,与对照组比较差异有统计学意义(P＜0.05).实验组细胞凋亡率为(18.93±1.41)％,对照组为(9.91±1.08)％,组间比较差异有统计学意义(P＜0.05).实验组穿越基质胶的细胞比例为(10.00±2.00)％,显著低于对照组(26.00±3.61)％,差异有统计学意义(P＜0.05).免疫印迹显示与对照组相比,T24ERα细胞内整合素β1、磷酸化FAK、磷酸化Src和Src蛋白表达明显减低. 结论 ERα通过下调整合素β1-FAK/Src信号通路抑制膀胱癌细胞的生长和转移,同时促进膀胱癌细胞的凋亡.
목적 탐토자격소수체α(ERα)대방광암세포증식화침습력적영향궤제. 방법 건립ERα과표체적방광암세포T24ERα모형,대조조위방광암세포주T24V공질립조.응용사갑기우담서비색법검측세포생장정황,류식세포기술검측세포조망정황,Transwell화세포화흔실험검측방광암세포적침습능력,단백질인적법검측ERα조절방광암세포증식화침습능력적신호통로. 결과 여공질립대조조상비,실험조재96 h화144 h세포억제솔분별위18.85％、37.21％,여대조조비교차이유통계학의의(P＜0.05).실험조세포조망솔위(18.93±1.41)％,대조조위(9.91±1.08)％,조간비교차이유통계학의의(P＜0.05).실험조천월기질효적세포비례위(10.00±2.00)％,현저저우대조조(26.00±3.61)％,차이유통계학의의(P＜0.05).면역인적현시여대조조상비,T24ERα세포내정합소β1、린산화FAK、린산화Src화Src단백표체명현감저. 결론 ERα통과하조정합소β1-FAK/Src신호통로억제방광암세포적생장화전이,동시촉진방광암세포적조망.
Objective To explore the function and mechanism of estrogen receptor α (ERα) in bladder cancer cell proliferation and aggressivity.Methods The ERα expression bladder cancer cell line T24ERα model was established.The cell growth was detected by MTT assay,apoptosis by flow cytometry,cell invasion by matrigel transwell.Western blot was used to check signals by ERα regulation in bladder cancer cells related to the proliferation and metastatic ability.Results Compared to the control group,the cell inhibition rates of experimental group in 96 h and 144 h were 18.85％ and 37.21％,respectively.The difference was significant compared with the control group (P ＜ 0.05).The apoptosis rates of the experimental group and control group were (18.93 ±1.41)％ and (9.91 ±1.08)％ (P＜0.05).The experimental group through matrix adhesive cell proportion was (10.00 ± 2.00)％,significantly lower than that of the control group (26.00 ± 3.61) ％ (P ＜ 0.05).Western blot showed integrin-β1,p-FAK,p-Src and Scr expression were reduced compared to control group (P ＜ 0.05).Conclusion ERα could inhibit bladder cancer cell growth and metastasis through down-regulating integrin-β1-FAK/Src signal pathway,while promote the apoptosis of bladder cancer cells.