浙江医学2018，Vol.40Issue(5)：443-447,5.DOI:10.12056/j.issn.1006-2785.2018.40.5.2017-1546
IL-32α抑制胰腺癌细胞上皮间质转化和侵袭转移作用机制研究
Effect of IL-32α on epithelial-mesenchymal transition and invasion/metastasis of pancreatic cancer cells and its mechanism
李冰震 1王理富 1吴文元 1陈景锋2
作者信息
- 1. 323000 丽水市人民医院(温州医科大学附属第六医院)急诊外科
- 2. 温州医科大学附属第一医院肝胆外科
- 折叠
摘要
Abstract
Objective To investigated the effects of IL-32α on epithelial mesenchymal transition (EMT),metastasis and invasion of human pancreatic cancer cell lines Panc-1 and AsPC-1 and the underlining mechanism.Methods Human pancreatic cancer Panc-1 and AsPC-1 cells were treated with different concentrations of IL-32 α in vitro.EMT related marks E-cadherin,Vimentinand Zeb1,and extracellular matrix metalloproteinases (MMP-2 and MMP-9) were detected by immunofluorescence staining,Western blotting and real-time PCR,respectively.The activation of Jak2/STAT3 signaling proteins was detected by Western blotting.Results The RT-PCR and West blot showed that expressions of vimentin,Zeb1,MMP-2,MMP-9,p-Jak2,Jak2 and p-STAT3 mRNA and/or proteins in Panc-1 and AsPC-1 cells were inhibited after treated with IL-32α for 24h in a dose-dependent manner (P＜0.05);the expression of E-cadherin was upregulated (P＜0.05),while total STAT3 levels were not changed(P ＞0.05).The immunofluorescence assay showed that the expression of vimentin was increased after IL-32α treatment in a dose-dependent manner.Conclusion IL-32α can inhibit the epithelial mesenchymal transition,reduce secretion of MMPs in a dose-dependent manner inPanc-1 and AsPC-1 cells,which is associated with the deactivation of Jak2/STAT3 signaling pathway.关键词
上皮间质转化/金属基质蛋白酶/IL-32α/Jak2/STAT3Key words
Epithelial mesenchymal transition (EMT)/Matrix metalloproteinases (MMPs)/Interleukin-32c(IL-32α)/Jak2/STAT3引用本文复制引用
李冰震,王理富,吴文元,陈景锋..IL-32α抑制胰腺癌细胞上皮间质转化和侵袭转移作用机制研究[J].浙江医学,2018,40(5):443-447,5.
