摘要
目的检测热休克蛋白75(Mortalin)在肝细胞癌中的表达,探讨其与血管生成和上皮间质转化(EMT)的关系。方法收集100例原发性肝癌(HCC)患者的癌组织和癌旁组织及10例正常肝组织,采用免疫组织化学染色、Western blot和qPCR检测Mortalin的表达,分析Mortalin表达与肝癌临床病理特征之间的关系。同时分析100例HCC患者癌组织中Mortalin、波形蛋白(Vimentin)和微血管密度(MVD)的表达情况,判断Mortalin的表达与EMT、肿瘤血管生成之间的关系。结果免疫组织化学显示Mortalin主要表达在细胞质中。肝癌组织中高表达Mortalin的比率是77%,显著高于癌旁组织的19%和正常组织的10%(χ2=67.388,16.669;P<0.01)。Mortalin的高表达与肝癌Edmondson分级、TNM分期、血管侵犯和淋巴结转移有关(P<0.05)。Western blot和qPCR检测结果显示肝癌组织中Mortalin相对含量明显高于癌旁和正常组织(P<0.05)。免疫组织化学染色检查显示,肝癌组织中Mortalin的表达与Vimentin的表达存在正相关(r=0.235,P<0.05),而高表达Mortalin的肝癌组织比低表达的有更高的MVD的趋势,但差异无统计学意义(t=1.630,P>0.05)。结论 Mortalin不能促进肝癌血管形成,但可能通过诱导肝癌组织的EMT而参与肝癌的侵袭和转移。
Objective To detect the expression of Heat shock protein 75 （ Mortalin ） in hepatocellular carcinoma （ HCC） ,and explore its relationship with angiogenesis and epithelial-mesenchymal transition （ EMT） . Methods A hundred cases of HCC tumor and paracarcinomatous tissues, and ten cases of normal liver tissues were collected. The expression of Mortalin and relationship between Mortalin and clinicopathological characteristics of HCC were detected and analyzed using immunohistochemistry, Western blot and qPCR. The expressions of Mortalin, Vimen-tin and microvessel density （ MVD） in 100 HCC tumor tissues were detected by immunohistochemistry, and then the relationship was judged between the expression of Mortalin, EMT and angiogenesis. Results Immunohisto-chemistry showed that Mortalin mainly expressed in the cytoplasm. The high expression rate of Mortalin in HCC tumor tissues was 77%, which was remarkably higher than that in paracarcinomatous tissues （ 19%） and normal liver tissues （ 10%） （χ2 =67. 388 , 16. 669;P〈0. 01 ） . The high expression of Mortalin in HCC was correlated with Edmondson grade, TNM stage, vascular invasion and lymph node metastasis （ P〈0. 05 ） . Western blot and qPCR analysis showed that relative content of Mortalin in HCC was significantly higher than that in paracarcinoma-tous and normal tissues （ P〈0. 05 ） . A significant positive correlation was found between the expression of Mortalin and Vimentin （ r=0. 235 , P〈0. 05 ） , but the high expression of Mortalin group had a tendency to higher MVD than that in low expression of Mortalin group （ t=1. 630 , P〉0. 05 ） . Conclusion The high expression of Mortalin can not promote angiogenesis, but may accelerate invasion and metastasis of HCC through inducing EMT.
出处
《安徽医科大学学报》
CAS
北大核心
2014年第6期795-799,共5页
Acta Universitatis Medicinalis Anhui
基金
国家自然科学基金(编号:81272398)
安徽省科技攻关计划项目(编号:12010402112)
安徽高校省级自然科学研究重点项目(编号:KJ2011A171)
作者简介
陈静，男，硕士研究生；
李建生，男，教授，主任医师，博士生导师，责任作者，E．mail：liianshengl953@163．com
