The effects of Runx2 on TGF-β1-induced epithelial-mesenchymal transition in lung cancer A549 cells

耿文文; 蒲　倩; 高海东

doi:10.19401/j.cnki.1007-3639.2019.09.001

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The effects of Runx2 on TGF-β1-induced epithelial-mesenchymal transition in lung cancer A549 cells

更新时间：2026-01-27

- The effects of Runx2 on TGF-β1-induced epithelial-mesenchymal transition in lung cancer A549 cells
- China Oncology Vol. 29, Issue 9, Pages: 681-687(2019)
- 作者机构：
  
  山东大学齐鲁医院（青岛）普外科,山东,青岛,266000
- 作者简介：
- 基金信息：
- DOI：10.19401/j.cnki.1007-3639.2019.09.001
  CLC： R734.2
- Published Online：20 November 2019，
  
  Published：20 November 2019
- 稿件说明：
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耿文文, 蒲　倩, 高海东. Runx2在TGF-β1诱导的肺癌A549细胞上皮-间质转化过程中的作用研究[J]. 中国癌症杂志, 2019, 29(9): 681-687.

耿文文, 蒲　倩, 高海东. The effects of Runx2 on TGF-β1-induced epithelial-mesenchymal transition in lung cancer A549 cells[J]. China Oncology, 2019, 29(9): 681-687.
耿文文, 蒲　倩, 高海东. Runx2在TGF-β1诱导的肺癌A549细胞上皮-间质转化过程中的作用研究[J]. 中国癌症杂志, 2019, 29(9): 681-687. DOI： 10.19401/j.cnki.1007-3639.2019.09.001.

耿文文, 蒲　倩, 高海东. The effects of Runx2 on TGF-β1-induced epithelial-mesenchymal transition in lung cancer A549 cells[J]. China Oncology, 2019, 29(9): 681-687. DOI： 10.19401/j.cnki.1007-3639.2019.09.001.

摘要

背景与目的：转化生长因子-β（transforming growth factor-β，TGF-β）通路与肿瘤细胞上皮-间质转化（epithelial-mesenchymal transition，EMT）过程有着密切的联系，而Runx2蛋白是TGF-β通路中重要的组成部分，与肿瘤的转移过程密切相关。探讨Runx2蛋白在TGF-β1诱导的肺癌A549细胞EMT过程中的作用。方法：利用TGF-β1诱导A549细胞（由天津医科大学附属肿瘤医院惠赠），建立EMT模型，通过利用RNA干扰及转染技术降低Runx2表达，研究其对肿瘤细胞EMT的影响，利用LY294002和PD98059分别阻断磷酸肌醇3激酶/蛋白激酶B（phosphatidylinositide3-kinases/protein kinase B，PI3K/AKT）和丝裂原活化蛋白激酶/细胞外信号调节激酶（mitogen-activated protein kinase/extracellular signal-regulated kinase，MAPK/ERK）通路研究Runx2作用的机制。结果：5 ng/mL TGF-β1 72 h可以诱导肺癌A549细胞发生明显的EMT，干扰Runx2的表达可以阻止TGF-β1诱导的肿瘤细胞发生EMT。在EMT过程中，TGF-Smad2通路及旁路PI3K/AKT和MAPK/ERK通路发生激活。通路实验显示，Runx2表达在PI3K/AKT通路阻断后明显降低。结论：Runx2在TGF-β1诱导的肿瘤细胞EMT过程中发挥着必要作用，而且TGF-β1主要是通过P13K/AKT通路调控Runx2的表达促进细胞发生EMT。

Abstract

Background and purpose: Transforming growth factor-β (TGF-β) signaling has been shown to play an important role in epithelial-mesenchymal transition (EMT). Furthermore

Runx2 plays an important role in the progress of tumor metastasis and is also regulated by TGF-β signaling. This study was designed to investigate the induction of EMT in response to TGF-β and the role of Runx2 in this process. Methods: A549 cells (donated by Tianjin Medical University Cancer Institute and Hospital) were induced by TGF-β1 to build the EMT model. The cells were infected with siRNA to downregulate the expression of Runx2. Phosphatidylinositide 3-kinases/protein kinase B (PI3K/AKT) and mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) pathway were blocked by specific inhibitor LY294002 and PD98059 to explore the mechanism. Results: The EMT model was induced by 5 ng/mL TGF-β1 for 72 h. At the same time

downregulation of Runx2 with siRNA could prevent cancer cell from the progress of EMT. In addition

the results showed PI3K/AKT-MAPK/ERK and TGF-β signaling pathways were both activated in this process

and the expression of Runx2 was significantly decreased after blocking PI3K/AKT pathway

compared with the MAPK/ERK pathway. Conclusion: TGF-β1 regulates Runx2 to affect the progression of EMT mainly by the PI3K/AKT pathway

and Runx2 plays a necessary role in the process of tumor cell EMT.

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