新基因JDP2通过不同通路抑制人胰腺癌上皮向间质转化作用的研究  

Effect of JDP2 on Epithelial-mesenchymal Transition in Human Pancreatic Cancer Cell Line

作　　者：许元鸿[1] 刘哲[1] 郭克建[1] 杜瑞霞[2] 蒋红军[3] 

机构地区：[1]中国医科大学附属第一医院胰腺外科,沈阳110001 [2]沈阳医学院附属奉天医院耳鼻咽喉科,沈阳110024 [3]沈阳医学院附属奉天医院放射线科,沈阳110024

出　　处：《中国医科大学学报》2012年第11期990-994,共5页Journal of China Medical University

基　　金：辽宁省科学技术计划项目(2011404013-4)

摘　　要：目的研究Jun二聚化蛋白2(JDP2)与人胰腺癌细胞系BxPC3上皮向间质转化(EMT)之间的关系。方法应用pCEFL-HA-JDP2质粒瞬时转染BxPC3细胞系,并继续分别用转化生长因子β1(TGF-β1)和I型胶原(Collagen I)诱导,以仅加DMSO为空白对照组,倒置显微镜观察细胞形态学变化,Western blot及免疫荧光检测E-cadherin、vimentin的表达。Transwell小室侵袭实验验证侵袭能力的变化。结果与空白对照组相比,转染JDP2组上皮标志物E-cadherin及间质标志物vimentin表达变化不明显,而转染空质粒组则E-cadherin表达降低而vimentin表达升高,提示JDP2能够抑制由Collagen I及TGF-β1诱导的EMT;同时我们验证,转染JDP2质粒组细胞侵袭能力亦明显小于转染空质粒组细胞(P<0.05)。结论 JDP2,作为AP-1类因子的抑制因子,可以通过不同通路抑制EMT的产生,从而为胰腺癌的分子靶向治疗找到新的方向。Objective To investigate the relationship of pancreatic cancer epithelial-to-mesenchymal transition（EMT） with the expression of Jun dimerization protein 2 （JDP2）. Methods The pancreatic cancer cell line BxPC3 was transfected with JDP2 and induced by Collagen I and TGF-131. Western blot analysis and immunofluorescence were performed to detect the protein expressions of the epithelial marker E-cad- herin and the mesenchymal marker vimentin. Cell migration was determined by Transwell motifity assay. Results After EMT induction, the E-cadherin and vimentin expression levels in JDP2 overexpressed cells did not change significantly compared with the non-induced cells （DMSO, negative control）, whereas E-cadherin expression decreased and vimentin expression increased in the vector control group cells. Ad- ditionally, compared with the negative control, only the BxPC3 cells transfected with empty plasmid showed significant morphological changes after Collagen I and TGF-β1 induction （P 〈 0.05）. Conclusion JDP2,as an AP-l-family inhibitor,inhibits EMT,which may lead to a new direction in molecular-targeted therapy for pancreatic cancer.

关 键 词：胰腺癌 转化生长因子Β1 胶原蛋白I 上皮向间质转化 Jun二聚化蛋白2 

分 类 号：R730.23[医药卫生—肿瘤]