STAT3和Cyclin D1在胰腺癌中的表达及其临床意义

目的探讨信号转导和转录激活因子-3(STAT3)、磷酸化STAT3(PSTAT3)及Cyclin D1 的蛋白在胰腺癌中表达情况及活化STAT3的蛋白表达与胰腺癌临床病理特征的关系。方法用免疫组化法检测41例手术切除的胰腺癌组织和10例正常胰腺组织中STAT3、PSTAT3、Cyclin D1的蛋白表达。结果在41例胰腺癌标本中有31例(75.6%)STAT3、29例(70.7%)PSTAT3和25例(61.0%) Cyclin D1的蛋白表达阳性,明显高于正常胰腺组织。STAT3主要在细胞质表达,PSTAT3和Cyclin D1 主要在细胞核内表达。PSTAT3和Cyclin D1蛋白的阳性表达呈正相关(P<0.001)。PSTAT3在临床分期较晚和有淋巴结转移的胰腺癌中呈高表达(P<0.05),Cyclin D1的表达与淋巴结转移有关(P< 0.05)。结论本研究结果表明胰腺癌组织中存在STAT3、PSTAT3和Cyclin D1的过表达,并与临床病理分期和淋巴结转移有关,PSTAT3过表达与Cyclin D1的表达呈正相关,提示PSTAT3可能通过上调Cyclin D1表达,在胰腺癌的发生发展中起重要作用。

Expression of STAT3 and Cyclin D1 in pancreatic carcinoma and clinical significance

Objective To investigate the expression of STAT3, PSTAT3 and Cyclin D1 and the relationship between PSTAT3 and various clinical pathological characteristics in human pancreatic carcinoma. Methods The expression of Cyclin Dl, STATS and its activated form PSTAT3 in tumor tissues from 41 radically resected specimens of pancreatic carcinoma and 10 normal pancreatic tissues was detected by immunohistochemical staining. Results The protein expression rate of STATS, PSTAT3 and Cyclin Dl in pancreatic carcinoma was 31/41(75. 6%), 29/41(70. 7%) and 25/41 (61. 0%) respectively, which were significantly higher than that in normal group (P < 0. 001). The positive rate of PSTAT3 was closely related to the clinical stage and lymph node metastasis (P < 0. 05). STATS in pancreatic carcinoma was located in the cytoplasm, while PSTAT3 and Cyclin Dl were located in the cell nucleus. There was a positive correlation between the positive rates of PSTAT3 and Cyclin D1 (P < 0. 01). Cyclin D1 was also related to lymph node metastasis(P < 0. 05). Conclusions STAT3, PSTAT3 and Cyclin D1 were overexpressed in human pancreatic carcinoma. Activation of STAT3 was significantly related to the clinical stage and lymph node metastasis. A positive correlation was found between the expression rates of PSTAT3 and Cyclin Dl. It is suggested that PSTAT3 might play an important role in the carcinogenesis and progress of pancreatic carcinoma via up-regulating the expression of Cyclin D1.