摘要
目的:研究第10号染色体上缺失的抑癌基因与张力蛋白同源的磷酸酯酶基因(phosphataseandtensinhomlogdeletedonchromosometenprotein,PTEN)与磷酸化丝氨酸/苏氨酸蛋白激酶B(phosphoserine/threonineproteinkinaseB,pAkt)在肝细胞癌(hepatocellularcarcinoma,HCC)中蛋白的表达、意义及两者相关性。方法:采用免疫组织化学法检测71例HCC及癌旁组织中PTEN和pAkt的表达。结果:1)HCC中PTEN蛋白阳性率(36.6%,26/71)明显低于癌旁肝组织(93.0%,66/71),P=0.000,且随HCC恶性程度升高而显著下降;2)pAkt在HCC中表达率(80.3%,57/71)明显高于癌旁肝组织(29.6%,21/71),P=0.000,且其表达率随HCC恶性程度升高而增加;3)HCC中PTEN与pAkt表达呈负相关,r=-0.307,P=0.009。结论:PTEN蛋白低表达不能有效抑制pAkt异常激活,从而对HCC发生、发展起重要作用。
OBJECTIVE： To study the expressions and signifieance of the tumor supressor gene phosphatase and tensin homlog deleted on chromosome ten protein（PTEN）and oncogene phosphoserine/ threonine protein kinase B（phospho-serine/threonine protein kinase, pAkt） in hepatocellular careinoma（HCC）, and analyze the relationship between PTEN and pAkt. METHODS： staining with SP methods were used to detect the expressions of PTEN and pAkt in 71 cases of HCC and their pericarcinomatous tissues. RESULTS：1）The positive expression rate of PTEN in HCC was lower than that in perieareinomatous liver tissues（36. 6% vs 93. 0%）, P= 0. 000. 2）The positive rate of pAkt expression in HCC was higher than that in perieareinomatous liver tissues （80. 3% vs 29. 6%）, P= 0. 000. With the progress of the tumor pathological differentiation and clinical stage, the positive rate of PTEN protein in HCC decreased; whereas that of pAkt was entirely contrary. 3） The expression of PTEN was negatively associated with that of pAkt （r=-0. 307, P= 0. 009） in HCC. ODNCLUSION： The mechanism that hypoexpression of PTEN can not inhibit abnormal activation of pAkt may play an im- portant role in the initiation and development of HCC.
出处
《中华肿瘤防治杂志》
CAS
2006年第1期51-54,57,共5页
Chinese Journal of Cancer Prevention and Treatment
基金
湖北省科技攻关计划资助项目(AA301C43)
作者简介
刘恩宇，男，山东邹城人，博士，主要从事肝胆外科临床科研工作。Tel：86-27-83663840 E-mail：liuenyu@163．com
