摘要
目的 探讨蛋白激酶C(PKC)及其抑制物 (PKCI)在膀胱移行细胞癌发生过程中的分子生物学机制。 方法 采用Takai法检测 2 0例膀胱移行细胞癌及癌周正常膀胱粘膜中PKC及其内源性抑制物 (PKCI)的活性。 结果 膀胱癌与癌周正常膀胱粘膜相比 ,胞膜 (8.6 7± 2 .0 7,10 .6 6± 1.2 4)、胞浆 (7.6 8± 3 .2 7,2 0 .6 3± 12 .77)及总体 (7.71± 4.5 2 ,14.34± 7.47)PKC活性 (pmol·mg-1·min-1)明显降低 (P <0 .0 5 ) ,胞膜 /胞浆PKC活性比率 (1.2 5± 0 .5 8,0 .44± 0 .32 )显著升高 (P <0 .0 1) ;膀胱癌与癌周正常膀胱粘膜相比 ,胞膜 (17.2 8± 7.2 2 ,10 .5 1± 4.85 )、胞浆 (2 1.86± 7.34,15 .88± 9.36 )PKCI活性明显升高 (P <0 .0 5 ) ,总体 (19.2 9± 5 .5 2 ,12 .6 2± 3.93)PKCI活性显著升高(P <0 .0 1) ,胞膜 /胞浆PKCI活性比率 (0 .83± 0 .34,0 .72± 0 .2 5 )无明显变化 (P >0 .0 5 )。 结论 PKC及PKCI在亚细胞水平的活性变化对膀胱移行细胞癌的发生起重要的调控作用 ,膀胱癌组织中PKC处于激活状态 。
Objective To study the molecule biological mechanism of PKC and PKC inhibitor (PKCI) on the carcinogenesis of bladder transitional cell carcinoma. Methods Takai method was followed to measure the activity of PKC and PKCI in 20 cases of bladder transitional cell carcinoma and in normal tissues around the tumor. Results Compared with that of the normal tissues around the tumor, PKC activity in carcinoma was reduced in the plasmic, membranous fraction and total tissue ( P <0.05);the ratio of membrane/plasm being increased significantly ( P <0.01). In addition, compared with that of the normal tissues around the tumor, PKCI activity in carcinoma increased in the plasmic and membranous fraction ( P <0.05)and increased significantly in total tissue ( P <0.01).Hence the ratio of membrane/plasm did not alter obviously ( P >0.05). Conclusions The activity of PKC and PKCI in sub cell level might play an important regulatory role in bladder carcinogenesis. PKC was activited in bladder carcinoma in a down regulation manner.
出处
《中华泌尿外科杂志》
CAS
CSCD
北大核心
2001年第3期148-150,共3页
Chinese Journal of Urology
基金
卫生部科学研究基金项目资助!(98 1189)