摘要目的 检测食管鳞癌组织中信号转导子和转录激活子3( STAT3)在mRNA、蛋白质和蛋白质磷酸化3种水平的表达,探讨其在食管鳞癌发生、发展、浸润、转移中的作用。方法 检测43例食管鳞癌组织中的STAT3 mRNA、STAT3和磷酸化STAT3( pSTAT3)的表达,并与相应癌旁正常食管组织作对照研究,分析STAT3 mRNA、STAT3和pSTAT3的表达与临床病理参数的关系。结果 43例实验样本中(1)食管鳞癌组织中STAT3 mRNA相对表达强度比值(1.43±0.59)较癌旁组织的比值(0.98±0.47)明显增高(P＜0.05);(2)食管鳞癌组织中STAT3、pSTAT3表达(2.16±0.39、1.40±0.15)也都显著高于癌旁组织(1.87±0.29、1.25±0.13,P＜0.05);(3)食管鳞癌组织中STAT3mRNA、STAT3和pSTAT3在肿瘤不同分化级别中表达差异有统计学意义,分化级别越低,表达水平越高(P＜0.05),并与肿瘤分化级别呈负相关(-1 ＜r＜-0.301,P＜0.05);它们在TNM分期中Ⅲ期组的表达均高于Ⅰ～Ⅱ期组(P＜0.05),伴有淋巴结转移组表达也都高于无淋巴结转移组(P＜0.05),并与两者呈正相关(两者均为0.301 ＜r＜1,P＜0.05);但未发现它们在性别、年龄、家族史、吸烟史中差异有统计学意义(P＞0.05)。结论 食管鳞癌组织中STAT3磷酸化异常激活后,导致STAT3mRNA、STAT3和pSTAT3的高表达,与食管鳞癌的分化、浸润、转移相关。

abstractsObjective By testing the expression of signal transducer and activator of transcription 3 (STAT3) in esophageal squamous cell carcinoma (ESCC) tissue at mRNA, protein and protein phosphorylation levels, to study the function of STAT3 in the occurrence, development, invasion and metastasis of ESCC. Methods By using adjacent normal esophageal tissue as control, the expression of STAT3 mRNA,STAT3 and phosphorylated STAT3 (pSTAT3) in 43 ESCC samples was detected to reveal the correlation with clinicopathological rarameters. Results In the 43 tested samples, ( 1 ) Remarkably higher relative expression intensity of STAT3 at mRNA was found in ESCC tissue ( 1.43 ±0. 59), than in normal esophageal tissue (0. 98 ± 0.47, P ＜ 0. 05 ) ; ( 2 ) STAT3 and pSTAT3 expression in ESCC (2. 16 ± 0. 39, 1.40 ±0. 15) was also significantly higher than in normal tissue ( 1.87 ± 0. 29, 1.25 ± 0. 13, P ＜ 0.05 ) ; ( 3 )Statistical differences were found in different differentiation degrees of tumor for the expression of STAT3 mRNA, STAT3 and pSTAT3 in ESCC. The lower differentiation degree was, the higher the expression (P ＜0. 05). The expression was negatively correlated with differentiation degree of tumor (-1 ＜ r ＜-0. 301 ,P＜ 0. 05 ), while it had a positive relationship with TNM staging and lymph node metastasis (0. 301 ＜r ＜ 1 ,P ＜0. 05). In TNM staging, higher expression was found in stage Ⅲ than in both stage Ⅰ and stage Ⅱ (P ＜ 0. 05 ), and the expression in the group with lymph node metastasis was higher than that in the group without lymph node metastasis ( P ＜ 0. 05 ). No obvious connection was found with the age,gender, family history and smoking history of patients (P ＞ 0. 05 ). Conclusion High expression of STAT3 mRNA, STAT3 and pSTAT3 in ESCC tissue was caused by the aberrant activation of STAT phosphorylation, which was closely related with the differentiation, invasion and metastasis of ESCC.