中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
CHINESE JOURNAL OF EXPERIMENTAL SURGERY
2011年
9期
1519-1522
,共4页
肖仁栋%涂远荣%陈剑锋%李旭%林敏%赖繁彩
肖仁棟%塗遠榮%陳劍鋒%李旭%林敏%賴繁綵
초인동%도원영%진검봉%리욱%림민%뢰번채
食管鳞癌%转录激活子3
食管鱗癌%轉錄激活子3
식관린암%전록격활자3
Esophageal squamous cell carcinoma%STAT3
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。
目的 檢測食管鱗癌組織中信號轉導子和轉錄激活子3( STAT3)在mRNA、蛋白質和蛋白質燐痠化3種水平的錶達,探討其在食管鱗癌髮生、髮展、浸潤、轉移中的作用。方法 檢測43例食管鱗癌組織中的STAT3 mRNA、STAT3和燐痠化STAT3( pSTAT3)的錶達,併與相應癌徬正常食管組織作對照研究,分析STAT3 mRNA、STAT3和pSTAT3的錶達與臨床病理參數的關繫。結果 43例實驗樣本中(1)食管鱗癌組織中STAT3 mRNA相對錶達彊度比值(1.43±0.59)較癌徬組織的比值(0.98±0.47)明顯增高(P<0.05);(2)食管鱗癌組織中STAT3、pSTAT3錶達(2.16±0.39、1.40±0.15)也都顯著高于癌徬組織(1.87±0.29、1.25±0.13,P<0.05);(3)食管鱗癌組織中STAT3mRNA、STAT3和pSTAT3在腫瘤不同分化級彆中錶達差異有統計學意義,分化級彆越低,錶達水平越高(P<0.05),併與腫瘤分化級彆呈負相關(-1 <r<-0.301,P<0.05);它們在TNM分期中Ⅲ期組的錶達均高于Ⅰ~Ⅱ期組(P<0.05),伴有淋巴結轉移組錶達也都高于無淋巴結轉移組(P<0.05),併與兩者呈正相關(兩者均為0.301 <r<1,P<0.05);但未髮現它們在性彆、年齡、傢族史、吸煙史中差異有統計學意義(P>0.05)。結論 食管鱗癌組織中STAT3燐痠化異常激活後,導緻STAT3mRNA、STAT3和pSTAT3的高錶達,與食管鱗癌的分化、浸潤、轉移相關。
목적 검측식관린암조직중신호전도자화전록격활자3( STAT3)재mRNA、단백질화단백질린산화3충수평적표체,탐토기재식관린암발생、발전、침윤、전이중적작용。방법 검측43례식관린암조직중적STAT3 mRNA、STAT3화린산화STAT3( pSTAT3)적표체,병여상응암방정상식관조직작대조연구,분석STAT3 mRNA、STAT3화pSTAT3적표체여림상병리삼수적관계。결과 43례실험양본중(1)식관린암조직중STAT3 mRNA상대표체강도비치(1.43±0.59)교암방조직적비치(0.98±0.47)명현증고(P<0.05);(2)식관린암조직중STAT3、pSTAT3표체(2.16±0.39、1.40±0.15)야도현저고우암방조직(1.87±0.29、1.25±0.13,P<0.05);(3)식관린암조직중STAT3mRNA、STAT3화pSTAT3재종류불동분화급별중표체차이유통계학의의,분화급별월저,표체수평월고(P<0.05),병여종류분화급별정부상관(-1 <r<-0.301,P<0.05);타문재TNM분기중Ⅲ기조적표체균고우Ⅰ~Ⅱ기조(P<0.05),반유림파결전이조표체야도고우무림파결전이조(P<0.05),병여량자정정상관(량자균위0.301 <r<1,P<0.05);단미발현타문재성별、년령、가족사、흡연사중차이유통계학의의(P>0.05)。결론 식관린암조직중STAT3린산화이상격활후,도치STAT3mRNA、STAT3화pSTAT3적고표체,여식관린암적분화、침윤、전이상관。
Objective 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.