CAJ | 학술논문

目的研究肝癌组织中二酰甘油激酶α( DGKα)和蛋白激酶C(PKC)的表达及临床意义.方法应用免疫组织化学法检测DGKα在60例肝癌组织、癌旁组织及10例正常肝组织中的表达,统计分析DGKα的表达与临床病理因素的关系.结果 DGKα和PKC在正常肝组织的阳性表达率最高,分别为90.0％(9/10)和100.0％(10/10),在肝癌组织中分别为81.7％(49/60)和71.7％(43/60),在癌旁组织中明显降低,分别为58.3％(35/60)和61.7％(37/60),三种肝组织中DGKα及KFC蛋白的表达阳性率差异有统计学意义(P＜0.05).正常肝组织、癌组织及癌旁组织中两蛋白表达部位逐渐从肝细胞胞质和(或)细胞核移至胞膜.肝癌组织中DGKα与PKC表达呈正相关(r=0.495,P＜ 0.05).DGKα阳性表达率与原发性肝癌的分化类型、是否有门静脉癌栓和TNM分期有关(均P＜0.05).结论分期越晚、分化越差的肝癌中DGKα的活性越强,DGKα可能促进了原发性肝癌的病理进程.
목적 연구간암조직중이선감유격매α( DGKα)화단백격매C(PKC)적표체급림상의의.방법 응용면역조직화학법검측DGKα재60례간암조직、암방조직급10례정상간조직중적표체,통계분석DGKα적표체여림상병리인소적관계.결과 DGKα화PKC재정상간조직적양성표체솔최고,분별위90.0％(9/10)화100.0％(10/10),재간암조직중분별위81.7％(49/60)화71.7％(43/60),재암방조직중명현강저,분별위58.3％(35/60)화61.7％(37/60),삼충간조직중DGKα급KFC단백적표체양성솔차이유통계학의의(P＜0.05).정상간조직、암조직급암방조직중량단백표체부위축점종간세포포질화(혹)세포핵이지포막.간암조직중DGKα여PKC표체정정상관(r=0.495,P＜ 0.05).DGKα양성표체솔여원발성간암적분화류형、시부유문정맥암전화TNM분기유관(균P＜0.05).결론 분기월만、분화월차적간암중DGKα적활성월강,DGKα가능촉진료원발성간암적병리진정.
Objective To investigate the expression and the clinical significance of diacylglycerol kinase α (DGKα) and protein kinase C (PKC) in human hepatocellular carcinoma (HCC).Methods DGKα and PKC expressions in the samples from 60 pathologically confirmed HCC patients were analyzed by immunohistochemistry. The relationship between DGKo expression and clinical pathology factors was analyzed.Results The expression positive rates of DGKo and PKC were highest in normal liver tissues [90.0％ (9/10) and 100.0％ (10/10)].The positive rates were 81.7 ％ (49/60) and 71.7 ％ (43/60) in HCC tissues,respectively,and were 58.3 ％ (35/60) and 61.7 ％ (37/60) in carcinoma adjacent tissues,respectively.In three liver tissues,the positive rates of DGKα and PKC were significantly different (P ＜0.05).The location of both kinases in hepatocytes translocated from cytoplasm/nucleus to membrane.The expressions of DGKα and PKC were positively correlation (r =0.495, P ＜ 0.05), The DGKα expression was correlated to differentiation type,portal venous tumor thrombus and TNM staging (all P ＜ 0.05).Conclusion DGKa is expressed with high activity in advanced stage and poorly differentiated HCC. It may be promote the pathological process of HCC.