LPS通过p38/MAPK调控胆管癌细胞系ICBD的上皮间质转化  

LPS regulates epithelialmesenchymal transition in cholangiocarcinoma cell line ICBD via the p38/MAPK signaling pathway

作　　者：李航宇[1] 李岩[1] 刘丹[1] 孙宏治[2] 刘金钢[1] 

机构地区：[1]中国医科大学附属盛京医院普通外科,辽宁省沈阳市110004 [2]辽宁医学院附属第一医院普通外科,辽宁省锦州市121001

出　　处：《世界华人消化杂志》2013年第21期2070-2075,共6页World Chinese Journal of Digestology

基　　金：国家自然科学基金面上资助项目;No.81071955;辽宁省教育厅科技项目计划基金资助项目;No.L2010634~~

摘　　要：目的:探讨脂多糖(lipopolysacoharides,LPS)对胆管癌细胞上皮间质转化(epithelial-mesenchymaltransition,EMT)的影响和可能机制.方法:将胆管癌ICBD细胞分为4组:正常对照组、LPS诱导实验组(终浓度10g/mL)、LPS+siRNA转染组和LPS+SB-203580诱导实验组.应用Real-time RT-PCR与Westernb l o t法检测上皮细胞表面标志E-钙黏蛋白(E-cadherin)和间质细胞表面标志波形蛋白(Vimentin)的表达变化以及Toll样受体4(Toll-like receptors4,TLR4)和p38的表达变化.结果:LPS促进胆管癌细胞系ICBD的EMT发生;ICBD细胞的EMT过程伴随TLR4、p38表达增加;应用siRNA阻断TLR4后,ICBD细胞的EMT消失,LPS导致p38的上调表达作用也消失;应用SB-203580阻断p38后,与正常对照组相比,TLR4的表达增加,与LPS诱导实验组相比无明显变化,但ICBD细胞的EMT消失.结论:LPS可以激活TLR4,并通过p38/MAPK促进胆管癌细胞ICBD的上皮间质转化.AIM： To investigate theffect of LPS on epitheli- al-mesenchymal transition （EMT） of cholangio- carcinoma ICBD cells and to explore the possible mechanisms involved. METHODS： ICBD cells were randomly divided into four groups： a control group, a LPS （finalconcentration, 10 pg/mL） group, a LPS ＋ siRNA group, and a LPS ＋ SB203580 group. The expres- sion of epithelial cell surface marker E-Cadherin, stromal cell surface marker Vimentin, TLR4 and p38 was examined by real-time RT-PCR and Western blot.RESULTS： LPS promoted the initiation of EMT of ICBD cells. The expression of TLR4 and p38 significantly increased in the process of EMT of ICBD cells. SiRNA-mediated blockage of TLR4 inhibited the occurrence of EMT and the up- regulation of p38 in ICBD cells. When p38 was blocked by SB-203580, the expression of TLR4 was still up-regulated, but EMT of ICBD cells did not occur compared to the control group.CONCLUSION： LPS may activate TLR4 and pro- mote EMT of cholangiocarcinoma cells via the p38/MAPK signaling pathway.

关 键 词：上皮间质转化 胆管癌细胞 脂多糖 Toll样受体4 P38 P38 MAPK 

分 类 号：R735.8[医药卫生—肿瘤]