| 摘要: |
| 目的观察IL-32α作用于人胰腺癌Panc-1、AsPC-1细胞后上皮间质转化（EMT）、侵袭转移及Jak2/STAT3信号通路的改变，并探讨其可能的作用机制。方法采用RT-PCR、Westernblot及细胞免疫荧光技术，检测不同浓度IL-32α处理24h后胰腺癌Panc-1、AsPC-1细胞的EMT相关标志物（E-cadherin、Vimentin、Zeb1）、侵袭转移相关分子标志物（MMP-2、MMP-9）mRNA与蛋白以及Jak2/STAT3信号通路相关蛋白p-Jak2、Jak2、p-STAT3、STAT3的表达情况。结果RT-PCR及Westernblot均显示胰腺癌Panc-1、AsPC-1细胞中E-cadherin的mRNA与蛋白表达水平均呈IL-32α剂量依赖性上调（均P＜0.05)；Vimentin、Zeb1、MMP-2及MMP-9的mRNA与蛋白表达水平均呈IL-32α剂量依赖性下调（均P＜0.05)；p-Jak2、Jak2、p-STAT3的表达水平均呈IL-32α剂量依赖性下调（均P＜0.05)，STAT3无明显改变（P＞0.05）。细胞免疫荧光染色显示Vimentin蛋白表达于细胞质中，且荧光强度呈IL-32α剂量依赖性下调（均P＜0.05)。结论IL-32α在一定剂量范围内以剂量依赖性的方式抑制胰腺癌Panc-1、AsPC-1细胞的EMT和侵袭转移，可能与抑制Jak2/STAT3信号通路有关。 |
| 关键词: 上皮间质转化 金属基质蛋白酶 IL-32α Jak2/STAT3 |
| DOI：10.12056/j.issn.1006-2785.2018.40.5.2017-1546 |
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| Effect of IL-32琢 on epithelial-mesenchymal transition and invasion/metastasis of pancreatic cancer cells and its mechanism |
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Lishui People's Hospital
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| 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-32α 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. |
| Key words: Epithelial mesenchymal transition (EMT) Matrix metalloproteinases (MMPs) Interleukin-32α(IL-32α)
Jak2/STAT3 |
