摘要
目的探讨Hedgehog信号通路重要成员Shh、Gli1、Sufu以及TAK1和磷酸化TAK1(p-TAK1)在胰腺癌组织中的表达及其与临床病理参数的相关性。方法应用免疫组化法检测38例手术切除的胰腺癌组织及其配对的癌旁胰腺组织中Shh、Gli1、Sufu、TAK1、P—TAK1蛋白的表达,分析它们与临床病理参数间的关系及它们相互间的关系。结果胰腺癌组织Shh、Gli1、Sufu、TAK1、P—TAK1蛋白的表达率分别为86.8%(33/38)、52.6%(20/38)、68.4%(26/38)、55.3%(21/38)、52.6%(20/38),而癌旁胰腺组织中的表达均为阴性。Gli1表达与肿瘤远处转移及临床分期呈正相关(r值分别为0.524、0.361,P值均〈0.05);Sufu表达与患者性别相关(r=-0.378,P〈0.05);TAK1表达与胰腺癌临床分期呈正相关(r=0.468,P〈0.05);p-TAK1表达与临床分期、肿瘤远处转移呈正相关(r值分别为0.418、0.361,P值均〈0.05)。胰腺癌组织中Gli1的表达水平与TAK1及p-TAK1呈正相关(P〈0.05)。结论Hedgehog信号通路及TAK1途径在胰腺癌的发生、发展中具有一定作用,且两条途径可能存在一定的相互作用。
Objective To investigate the expression of Hedgehog signaling pathway members, Shh, Glil, Sufu and TAK1 as well as phosphorylation-TAK1 (p-TAK1) protein in human pancreatic carcinoma tissues and to explore its relationship between the expression of proteins and the clinicopathologic parameters. Methods The expressions of Shh, Gill, Sufu, TAK1, p-TAK1 proteins in 38 samples of pancreatic cancer tissues and pairing adjacent normal pancreatic tissues were detected by immunohistoehemical method. The relationship among the proteins and the relationship between the expression of the proteins and the clinicopathologic parameters were examined. Results The positive expression rates of Shh, Glil, Sufu, TAK1, p-TAK1 protein in human pancreatic carcinoma were 86.8% ( 33/38 ), 52.6% (22/38), 68.4% (26/38), 55.3% (21/38), 52.6% (20/38), but they were not expressed in adjacent normal pancreatic tissues. Gift expression was positively related to distant metastasis and clinical staging (r =0. 524, 0.361, P 〈 0.05), Sufu expression was positively related to patient' s gender ( r = - 0. 378, P 〈 0.05 ), TAKI expression was positively related to clinical staging (r = 0.468, P 〈 0.05), p-TAK1 expression was positively related to clinical staging and distant metastasis ( r = 0. 418, 0. 361, P 〈 0.05). Glil expression was positively related to TAK1 and p-TAK1 expression in pancreatic cancer tissues (P 〈 0.05 ). Conclusions Hedgehog signaling pathway and p-TAK1 may play a role in the pathogenesis of pancreatic cancer, and the two pathways may interact with each other.
出处
《中华胰腺病杂志》
CAS
2013年第4期240-243,共4页
Chinese Journal of Pancreatology
基金
重大国际合作项目(30910103911)