PAFAH1B3介导上皮间质转化促进大细胞肺癌的转移

PAFAH1B3 Promotes Metastasis of Large Cell Lung Cancer by Regulating Epithelial-to-Mesenchymal Transition

目的研究血小板活化因子乙酰水解酶1b催化亚基3(PAFAH1B3)在大细胞肺癌(LCLC)中的作用及机制。方法Western blot法检测LCLC细胞中PAFAH1B3的表达。CCK8、克隆形成实验、Transwell实验和流式细胞术分别用于检测PAFAH1B3对H460细胞增殖、克隆形成、侵袭和细胞周期的影响。Western blot法分析沉默PAFAH1B3后E-cadherin和N-cadherin的表达变化。结果与人支气管上皮细胞相比,H460细胞中PAFAH1B3的蛋白表达水平明显升高。沉默PAFAH1B3显著抑制了H460细胞的增殖、克隆形成和侵袭能力。PAFAH1B3缺失情况下,H460细胞的细胞周期由S期向G_(0)/G_(1)期转化。机制研究发现,PAFAH1B3沉默后,H460细胞中E-cadherin蛋白表达显著上调,N-cadherin蛋白表达显著下调。结论PAFAH1B3在LCLC中发挥着致癌的作用,其可能通过调控上皮间质转化(EMT)过程促进了LCLC的转移。

Objective To investigate the effect and mechanism of platelet activating factor acetylhydrolase 1 b catalytic subunit 3(PAFAH1 B3)in large cell lung cancer(LCLC).Methods The expression of PAFAH1 B3 was detected by Western blotting in LCLC cells.CCK8,clone formation assay,Transwell assay and flow cytometry were used to detect the effects of PAFAH1 B3 on proliferation,clone formation,invasion and cell cycle in H460 cells,respectively.Western blotting was used to evaluate the changes of E-cadherin and N-cadherin expression after silencing PAFAH1 B3.Results The protein expression of PAFAH1 B3 was significantly elevated in H460 cells compared with human bronchial epithelial cells.Silencing of PAFAH1 B3 significantly inhibited proliferation,clone formation and invasion ability of H460 cells.In the absence of PAFAH1 B3,the cell cycle of H460 cells was transformed from S phase to G_(0)/G_(1) phase.Mechanistic studies revealed that the protein expression of E-cadherin was remarkably upregulated and the protein expression of N-cadherin was remarkably downregulated in H460 cells after PAFAH1 B3 silencing.Conclusion PAFAH1 B3 plays an oncogenic role in LCLC,and it can promote LCLC metastasis by regulating the epithelial-to-mesenchymal transition(EMT)process.