摘要
目的:探讨口腔鳞癌发生的分子生物学机理。方法:采用Takai法研究20例口腔鳞癌及其临近正常组织的蛋白激酶C(ProteinkinaseC,PKC)及其抑制物(ProteinkinaseCinhibitor,PKCI)活性。结果:与临近正常组织相比口腔鳞癌胞浆PKC活性明显升高(P<0.01),而胞膜无明显变化(P>0.05);与临近正常组织相比口腔鳞癌胞浆PKCI活性明显降低(P<0.01),而胞膜无明显变化(P>0.05)。结论:口腔鳞癌的发生与PKC及PKCI在亚细胞水平活性变化密切相关。
Objective: The paper was to explore the mocular mechanism of canceration in oral squamous cell carcinomas. Methods: We used Takai's method to study activity of protein kinase C (PKC) and its inhibitor (PKCI) in oral squamous cell carcinomas and their adjacent normal tissues from twenty patients. Results: The activity of PKC increased significantly (P<0.01) and that of PKCI decreased obviously (P<0.01) in cancerous cytoplasm as compared with that in adjacent tissues. No apparent change occured in cancerous cell membrane for the activity of PKC and PKCI in comparison with that in normal cells (P>0.05). Conclusions: The activity of PKC and PKCI was closely related to the canceration of the oral squamous cell carcinomas.
出处
《中国医科大学学报》
CAS
CSCD
北大核心
1998年第6期622-624,共3页
Journal of China Medical University
基金
辽宁省自然科学基金
关键词
口腔粘膜肿瘤
鳞癌
蛋白激酶C
抑制物活性
oral cavity
squamous cell carcinoma
protein kinase C
protein kinase C inhibitor
activity