摘要
目的:研究热休克蛋白(HeatShockProtein,HSP)90在乳腺癌细胞株ZR-75-30中的表达及对该细胞粘附侵袭能力的影响,并探讨相关机制及意义。方法:体外培养ZR-75-30乳腺癌细胞株,以HSP90抑制剂Geldanamycin(GA)作用处理;免疫印迹技术(Western-blot)检测GA处理前后HSP90在乳腺癌细胞株ZR-75-30中的表达情况;噻唑兰比色(MTT)法检测GA对ZR-75-30细胞的增殖抑制作用;噻唑兰比色(MTT)法检测细胞对人工基底膜(Matrigel)的粘附能力变化;TranswellCham-ber法观察癌细胞侵袭、迁移能力的改变。结果:HSP90抑制剂GA对ZR-75-30细胞具有增殖抑制作用,呈时间剂量依赖关系;GA作用后HSP90在乳腺癌细胞株ZR-75-30中表达明显下降;HSP90抑制剂GA处理的乳腺癌细胞ZR-75-30的粘附率较未加GA的对照组下降明显(P<0.01);在GA未处理对照组侵袭、迁移实验穿膜细胞数分别为95.4±5.2,103±15.4与GA处理实验组穿膜细胞数46.2±4.9,52.4±8.4相比具有显著性差异(P<0.01)。结论:通过抑制HSP90在乳腺癌细胞株ZR-75-30中的表达,GA能明显减弱乳腺癌细胞株ZR-75-30增殖粘附侵袭能力,HSP90与乳腺癌细胞增殖侵袭转移能力相关。
Objective:To investigate the expression and effect on invasion and metastasis of HSP90 in human breast cancer cell line ZR-75-30 in vitro and the mechanism of anti-invasion. Methods: The protein expression level of HSP90 in ZR-75-30 before and aftertreatment with HSP90 inhibitor GeManamycin was detected by Western-blotting; The effects of GA on the proliferation, invasion andmotility of human breast cancer cell line ZR-75-30 in vitro were explored respectively by MTT colorimetric assay and transwell chamber.Results: After treatment with GA the protein expression level of HSP90 in ZR-75-30 was decreased, and the proliferation of ZR-75-30cells was obviously inhibited in a dose and time-dependent manner. Compared with the control gnoup, the adhesion, invasion and motilityabilities of the ZR-75-30 cells were decreased significantly (P〈0.01). Conclusion:The results showed that The proliferation and invasiveability of the human breast cancer cell line ZR-75-30 can be suppressed by Geldanamycin and heat shock protein (HSP) 90 is associatedwith the invasive and metastatic abilities of breast cancer cell.
出处
《重庆医科大学学报》
CAS
CSCD
2006年第3期322-325,共4页
Journal of Chongqing Medical University
基金
重庆医科大学创新基金(No.cx200319)