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雷公藤甲素通过 ERK 通路诱导肺癌 A549细胞自噬

王伟 王坤

中国病理生理杂志2016,Vol.32Issue(9):1551-1555,5.
中国病理生理杂志2016,Vol.32Issue(9):1551-1555,5.DOI:10.3969/j.issn.1000-4718.2016.09.003

雷公藤甲素通过 ERK 通路诱导肺癌 A549细胞自噬

Tripchlorolide activates p-ERK and induces autophagy in lung cancer A549 cells

王伟 1王坤2

作者信息

  • 1. 杭州市下沙医院药学部,浙江 杭州 310018
  • 2. 杭州市下沙医院神经外科,浙江 杭州 310018
  • 折叠

摘要

Abstract

AIM: To investigate the effects of tripchlorolide (TP) on proliferation and autophagy of human lung cancer A549 cells, and explore its mechanism.METHODS: MTT assay was performed to analyze the effect of TP on the viability of human lung cancer A549 cells.The A549 cells were treated with TP, and their autophagy was observed un-der the fluorescence microscope through acridine orange staining.Green fluorescence spots were observed by fluorescence microscopy through GFP-LC3 plasmid transfection experiment.The levels of LC3 and p-ERK in the A549 cells after TP treatment were determined by Western blot.RESULTS: The viability of human lung cancer A549 cells was significantly inhibited by TP in a dose-time dependent manner (P <0.05).The number of the intracellular acidic follicles dyed with bright red fluorescence was significantly increased after TP treatment in A549 cells.The number of green dot-like con-gregate autophagosomes in cell cytoplasm was significantly increased after TP treatment in the A549 cells transfected with GFP-LC3 plasmid, while the normal treatment only induced a few cells with autophagosome formation.At the same time, we did not observe the dot-like congregate autophagosomes after TP treatment in the A549 cells transfected with GFP-control plasmid.Compared with control group, the expression of LC3-II protein was up-regulated in A549 cells after TP treatment (P <0.01).Furthermore, treatment with TP in A549 cells for 48 h also led to a significant upregulation of phosphorylated form of ERK (P <0.01).In contrast, no significant change in the levels of total ERK protein was observed.Compared with 100 nmol/L TP group, TP +3-MA group down-regulated the protein levels of LC3-II (P <0.01) and p-ERK (P <0.01) in the A549 cells.CONCLUSION: TP significantly inhibits the growth of A549 lung cancer cells and induces the <br> autophagy, which may be correlated with upregulation of p-ERK protein.

关键词

肺癌/雷公藤甲素/细胞增殖/自噬

Key words

Lung cancer/Tripchlorolide/Cell proliferation/Autophagy

分类

医药卫生

引用本文复制引用

王伟,王坤..雷公藤甲素通过 ERK 通路诱导肺癌 A549细胞自噬[J].中国病理生理杂志,2016,32(9):1551-1555,5.

基金项目

国家自然科学基金资助项目(No.81402044);浙江省自然科学基金资助项目 ()

中国病理生理杂志

OA北大核心CSCDCSTPCD

1000-4718

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