PTEN、p-Akt在肝癌组织中的表达及其与上皮间质转化的关系  

Expression of PTEN and p-Akt in Hepatocelluar Carcinoma and Their Relationship with Epithelial-mesenchymal Transitions

作　　者：张勇[1] 汤小玉 李荣清[1] 冯旭东[1] 张燕华[1] 王丽[2] 

机构地区：[1]昆明医科大学第一附属医院肿瘤放疗科,昆明650032 [2]成都军区昆明总医院病理科

出　　处：《西南国防医药》2014年第4期349-352,共4页Medical Journal of National Defending Forces in Southwest China

基　　金：国家自然科学基金项目(81201759);云南省应用基础研究项目(2012FB210)

摘　　要：目的探讨抑癌基因PTEN及其下游调控因子磷酸化Akt(p-Akt)在肝癌组织中的表达,并以上皮表型Ecadherin和间质表型Snail为标志,研究PTEN与上皮间质转化(EMT)在肝癌恶性进展过程中的作用。方法采用免疫组化EnVision法,检测80例肝细胞肝癌组织中PTEN、p-Akt、E-cadherin及Snail的表达情况,分析PTEN与p-Akt、Snail及E-cadherin表达的相关性。结果在肝癌组织中,PTEN、p-Akt、E-cadherin及Snail的表达率分别为46.25%、42.50%、67.50%及33.75%。PTEN、E-cadherin的表达率随着病变的进展而降低;而p-Akt和Snail的表达模式与PTEN、E-cadherin相反,表达率随着肝癌组织病变的进展而升高。Spearman相关分析显示,PTEN的表达与p-Akt、Snail的表达呈负相关(r值分别为-0.696、-0.291,P<0.05),与E-cadherin的表达呈正相关(r=0.537,P<0.05);Snail的表达与E-cadherin的表达呈负相关(r=-0.464,P<0.05)。结论肝癌的恶性进展可能与PTEN表达缺失导致的PI3K/AKT通路持续活化,进而促进EMT的发生有关;以PTEN为靶点提高其在肝癌组织中的表达,有望成为拮抗EMT、抑制肝癌恶性进展的新途径。Objective To investigate the expression of PTEN and p-Akt in hepatoeelluar carcinoma（HCC） and the correlation between PTEN and epithelial-mesenchymal transition（ EMT） in HCC malignant progression. Methods Immunohistochemical Envision method was applied in detecting the expressions of PTEN, pAkt, E-cadherin and Snail in 80 cases with HCC and the correlation among them was analyzed. Results The positive expression rate of PTEN, pAkt, E-cadherin and Snail in HCC was 46.25% （ 37/80）, 42.50% （34/80） ,67.50% （54/80） and 33.75 % （ 27/80 ）, respectively. The expression rates of PTEN and E-cadherin decreased in HCC malignant progression while the expression rates of pAkt and Snail increased;related analysis by Spearman pointed out that there existed a negative correlation between the expression of PTEN and those of pAkt and Snail （ r = - 0.696 and - 0.291, P 〈 0.05）, while a positive correlation between the expression of PTEN and that of E-cadherin（ r =0.537 ,P 〈0.05 ） ;there existed a negative correlation between the expression of Snail and that of E-cadherin（ r = - 0.464, P 〈 0.05 ）. Conclusions The defective expression of PTEN leads to a continuous activation of PI3K/AKT pathway that further promotes the occurrence of EMT,which may be of relationship with HCC malignant progression;to increase the expression of PTEN may be a hopeful new approach in antagonizing EMT and inhibiting the malignant procession of HCC.

关 键 词：肝癌 上皮间质转化 表达 

分 类 号：R735.7[医药卫生—肿瘤]