中华消化杂志
中華消化雜誌
중화소화잡지
Chinese Journal of Digestion
2011年
9期
604-608
,共5页
周琳%姚玮艳%张连峰%章永平%乔敏敏%袁耀宗
週琳%姚瑋豔%張連峰%章永平%喬敏敏%袁耀宗
주림%요위염%장련봉%장영평%교민민%원요종
胰腺肿瘤%肿瘤转移%微丝蛋白质类%RNA,小分子干扰%免疫组织化学%转染%肿瘤细胞.培养
胰腺腫瘤%腫瘤轉移%微絲蛋白質類%RNA,小分子榦擾%免疫組織化學%轉染%腫瘤細胞.培養
이선종류%종류전이%미사단백질류%RNA,소분자간우%면역조직화학%전염%종류세포.배양
Pancreatic neoplasms%Neoplasm metastasis%Microfilament proteins%RNA,small interfering%lmmunohistochemistry%Transfection%Tumor cells,cultured
目的 探讨骨架相关蛋白Transgelin在伴或不伴糖尿病的胰腺癌组织中的表达,及其对胰腺癌SW1990细胞运动侵袭的影响。方法 采用免疫组织化学法检测Transgelin在92例胰腺癌患者(其中伴糖尿病者45例)的癌组织、癌旁组织(距癌边缘>5 cm)中的表达水平,分析其与临床病理特征的关系;设计并体外合成靶向Transgelin的小干扰RNA(siRNA),将其转染到SW1990细胞中,采用Transwell小室检测转染前后细胞运动侵袭能力的改变。结果 Transgelin在胰腺癌 组织中的表达阳性率为68.5%(63/92),显著高于癌旁组织[33.7%(31/92),P<o.05]。伴随糖尿病的胰腺癌组织中Transgelin表达阳性率为84.4%(38/45),显著高于无糖尿病的胰腺癌组[53.2%(25/47),P<0.05]。胰腺癌组织中Transgelin表达与胰腺癌的淋巴结转移及TNM分期密切相关(P<0.05),与性别、年龄、发生部位、分化程度、门静脉或神经受侵犯无关(P>0.05)。Transgelin siRNA干扰后48 h,SW1990细胞迁移能力[穿膜细胞数为(49.2±9.5)个]明显低于阴性对照组和空白组[(61.9±7.5)和(65.3±10.6)个,P值均<0.05];SW1990细胞的体外侵袭能力[穿膜细胞数为(48.0±8.6)个]也明显低于阴性对照组和空白组[(63.5±11.4)个和(67.5±9.6)个,P值均<0.05]。结论 Transgelin可能通过促进胰腺癌细胞的运动侵袭能力,参与伴随糖尿病的胰腺癌的转移发生。
目的 探討骨架相關蛋白Transgelin在伴或不伴糖尿病的胰腺癌組織中的錶達,及其對胰腺癌SW1990細胞運動侵襲的影響。方法 採用免疫組織化學法檢測Transgelin在92例胰腺癌患者(其中伴糖尿病者45例)的癌組織、癌徬組織(距癌邊緣>5 cm)中的錶達水平,分析其與臨床病理特徵的關繫;設計併體外閤成靶嚮Transgelin的小榦擾RNA(siRNA),將其轉染到SW1990細胞中,採用Transwell小室檢測轉染前後細胞運動侵襲能力的改變。結果 Transgelin在胰腺癌 組織中的錶達暘性率為68.5%(63/92),顯著高于癌徬組織[33.7%(31/92),P<o.05]。伴隨糖尿病的胰腺癌組織中Transgelin錶達暘性率為84.4%(38/45),顯著高于無糖尿病的胰腺癌組[53.2%(25/47),P<0.05]。胰腺癌組織中Transgelin錶達與胰腺癌的淋巴結轉移及TNM分期密切相關(P<0.05),與性彆、年齡、髮生部位、分化程度、門靜脈或神經受侵犯無關(P>0.05)。Transgelin siRNA榦擾後48 h,SW1990細胞遷移能力[穿膜細胞數為(49.2±9.5)箇]明顯低于陰性對照組和空白組[(61.9±7.5)和(65.3±10.6)箇,P值均<0.05];SW1990細胞的體外侵襲能力[穿膜細胞數為(48.0±8.6)箇]也明顯低于陰性對照組和空白組[(63.5±11.4)箇和(67.5±9.6)箇,P值均<0.05]。結論 Transgelin可能通過促進胰腺癌細胞的運動侵襲能力,參與伴隨糖尿病的胰腺癌的轉移髮生。
목적 탐토골가상관단백Transgelin재반혹불반당뇨병적이선암조직중적표체,급기대이선암SW1990세포운동침습적영향。방법 채용면역조직화학법검측Transgelin재92례이선암환자(기중반당뇨병자45례)적암조직、암방조직(거암변연>5 cm)중적표체수평,분석기여림상병리특정적관계;설계병체외합성파향Transgelin적소간우RNA(siRNA),장기전염도SW1990세포중,채용Transwell소실검측전염전후세포운동침습능력적개변。결과 Transgelin재이선암 조직중적표체양성솔위68.5%(63/92),현저고우암방조직[33.7%(31/92),P<o.05]。반수당뇨병적이선암조직중Transgelin표체양성솔위84.4%(38/45),현저고우무당뇨병적이선암조[53.2%(25/47),P<0.05]。이선암조직중Transgelin표체여이선암적림파결전이급TNM분기밀절상관(P<0.05),여성별、년령、발생부위、분화정도、문정맥혹신경수침범무관(P>0.05)。Transgelin siRNA간우후48 h,SW1990세포천이능력[천막세포수위(49.2±9.5)개]명현저우음성대조조화공백조[(61.9±7.5)화(65.3±10.6)개,P치균<0.05];SW1990세포적체외침습능력[천막세포수위(48.0±8.6)개]야명현저우음성대조조화공백조[(63.5±11.4)개화(67.5±9.6)개,P치균<0.05]。결론 Transgelin가능통과촉진이선암세포적운동침습능력,삼여반수당뇨병적이선암적전이발생。
Objective To investigate the expression of actin-associated protein Transgelin in pancreatic cancer with or without diabetes and its effects on migration and invasion in SW1990 cell line. Methods The expression of Transgelin in 92 pancreatic cancer tissue specimens (45 cases accompanied with diabetes) and adjacent tumor-free tissue specimens (over 5cm from the edge of the tumor) was detected by immunohistochemistry, and their association with clinical pathological characteristics were also analyzed. Transgelin siRNA was designed and transfected into pancreatic cancer cell line SW1990. The changes of migration and invasion before and after transfection were observed through Transwell test.Results The positive percentage of Transgelin expression in pancreatic cancer was 68.5 % (63/92), which was significantly higher than that of adjacent tumor-free tissues[33.7% ( 31/92), P< 0.05]. The positive percentage of Transgelin expression in pancreatic cancer accompanied with diabetes was 84.4% (38/45), which was significantly higher than that without diabetes[53.2% (25/47), P<0.05]. The expression of Transgelin in pancreatic cancer tissues was associated with lymph nodes metastasis and TNM staging (both P<0.05), but not related with gender, age, site, differentiation and portal vein or nerve invasion (P>0.05). After Transgelin was interfered for 48 hours, the migration ability was significantly lower (migration cell number 49.2 ±9.5 cells) than negative control group (61.9±7.5 cells) and blank group (65.3±10.6 cells) (both P<0.05), and the invasion of SW 1990 cells (48.0 ± 8.6 cells) also significantly lower than negative control group (63.5±11.4 cells) and blank group (67.5±9.6 cells) (both P<0. 05). Conclusion Transgelin may involve in the metastasis of pancreatic cancer accompanied with diabetes through promoting pancreatic cancer cell migration and invasion.