OPN和Syndecan-1在原发性肝癌中的表达及与临床病理参数之间的相关性

目的:应用组织芯片技术考察骨桥蛋白(osteopontin,OPN)和Syndecan-1在原发性肝细胞癌(hepatocellular carcinoma,HCC)中的表达及与临床病理参数之间的相关性,分析两者在HCC发生发展过程中的可能机制.方法:应用S-P法对高通量肝癌组织芯片(478点阵,产品批号:OD-CT-DgLiv01-001)进行染色,检测OPN和Syndecan-1蛋白在肝癌、肝硬化和正常肝组织中的表达.结果:OPN在HCC、肝硬化和正常肝组织中的阳性率分别为73.3%,47.4%和22.2%,差异具有显著性(P<0.05,P<0.05);Syndecan-1在HCC、肝硬化和正常肝组织中的阳性率分别为19.6%,35.0%和90%,亦有显著性差异(P<0.05,P<0.01).单因素分析结果显示OPN的表达与肿瘤包膜的完整性(x~2=4.52,P<0.05),门静脉有无癌栓(x~2=4.28,P<0.05)及肿瘤的转移相关(x~2=7.21,P<0.05),与其他临床病理特征没有相关性;Syndecan-1的表达与肿瘤有无包膜(x~2=5.58,P<0.01),病理分级(x~2=4.35,P<0.01)以及肿瘤转移与否相关(x~2=3.37,P<0.05),与其他临床病理特征没有相关性.蛋白之间的相关性分析显示,OPN与Syndecan-1之间存在负相关(r=-0.439,P<0.01).结论:组织芯片是一种可高效率和高通量研究肿瘤分子病理的技术平台;HCC的发生发展与癌细胞OPN的过表达和Syndecan-1表达下调可能有关,OPN可能通过下调Syndecan-1的表达,降低肿瘤细胞之间的黏附性,从而促进肿瘤的转移.

Study on the expression of Osteopontin and Syndecan-1 and their correlations with the clinical pathological characteristics of hepatocellular carcinoma by tissue microarray technique

AIM:To explore the expression of osteopontin (OPN)and syndecan-1 as well as their correlations with the clinical pathological characteristics of hepatocellular carcinoma (HCC)by tissue microarray(TMA)technique, and analyze the potential mechanisms during the development and progression of HCC. METHODS:The expression patterns of OPN and syndecan-1 proteins in HCC,liver cirrhosis (LC)and normal liver tissue(NLT)were inves- tigated using high throughput TMA specified to HCC(478 spots,product batch No:OD-CT- DgLiv01-001)by SP method. RESULTS:The positive rate of OPN in HCC was significantly higher than that in LC or NLT (73.3% vs 47.4%,22.2%,both P<0.05).Corre- spondingly,the positive rate of Syndecan-1 ex- pression was significantly lower than that in LC or NLT(19.6% vs 35.0%,90.0%,P<0.05,P<0.01). The results of single-factor analysis showed that OPN expression was correlated with the inte- grality of tumor membrane(x~2=4.52,P<0.05), the formation of embolus in portal vein(x~2= 4.28,P<0.05)and metastases(x~2=7.21,P<0.05). Syndecan-1 expression was correlated with the integrality of tumor membrane(x~2=5.58,P<0.01),metastases(x~2=3.37,P<0.05)and patho- logical grades(x~2=4.35,P<0.01).Moreover, OPN was negatively correlated with syndecan-1 (r=-0.439,P<0.01). CONCLUSION:TMA is a high-throughput plat- form by which molecular pathology of cancer can be studied effectively.Over-expression of OPN and down-regulation of syndecan-1 may be involved in the development and progression of HCC,suggesting that OPN may decrease the adhesiveness of tumor cells and promote the metastasis by down-regulating the expression of syndecan-1.