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Article

Atorvastatin partially inhibits the epithelial-mesenchymal transition in A549 cells induced by TGF-β1 by attenuating the upregulation of SphK1

  • Authors:
    • Zhiqiang Fan
    • Handong Jiang
    • Zili Wang
    • Jieming Qu
  • View Affiliations / Copyright

    Affiliations: Department of Pulmonary Medicine, Huadong Hospital, Shanghai Medical College, Fudan University, Shanghai 200040, P.R. China, Department of Pulmonary Medicine, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200127, P.R. China, Department of Chemotherapy, The First Affiliated Hospital of Fujian Medical University, Fuzhou 350005, P.R. China, Department of Pulmonary Medicine, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200025, P.R. China
  • Pages: 1016-1022
    |
    Published online on: June 22, 2016
       https://doi.org/10.3892/or.2016.4897
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Abstract

Statins are the most effective drugs used in the reduction of intracellular synthesis of cholesterol. Numerous studies have confirmed that statins reduce the risk of multiple types of cancers. Statin use in cancer patients is associated with reduced cancer-related mortality. Epithelial-to-mesenchymal transition (EMT), a complicated process programmed by multiple genes, is an important mechanism of cancer metastasis. We explored the effect and mechanism of atorvastatin on the EMT process in A549 cells by establishing an EMT model in vitro induced by TGF-β1, and evaluated the effects of atorvastatin on the lower signaling pathway of TGF-β1 stimulation. Our results showed that atorvastatin partially inhibited the EMT process, and inhibited cell migration and actin filament remodeling. Transcriptional upregulation of ZEB1 and protein sphingosine kinase 1 (SphK1) induced by TGF-β1 was also suppressed. SphK1 plasmid transient transfection strengthened the EMT process induced by TGF-β1 in the presence of atorvastatin. Our experiments confirmed that atorvastatin can partially inhibit the EMT process of non-small cell lung cancer cells induced by TGF-β1 by attenuating the upregulation of SphK1.
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Copy and paste a formatted citation
Spandidos Publications style
Fan Z, Jiang H, Wang Z and Qu J: Atorvastatin partially inhibits the epithelial-mesenchymal transition in A549 cells induced by TGF-β1 by attenuating the upregulation of SphK1. Oncol Rep 36: 1016-1022, 2016.
APA
Fan, Z., Jiang, H., Wang, Z., & Qu, J. (2016). Atorvastatin partially inhibits the epithelial-mesenchymal transition in A549 cells induced by TGF-β1 by attenuating the upregulation of SphK1. Oncology Reports, 36, 1016-1022. https://doi.org/10.3892/or.2016.4897
MLA
Fan, Z., Jiang, H., Wang, Z., Qu, J."Atorvastatin partially inhibits the epithelial-mesenchymal transition in A549 cells induced by TGF-β1 by attenuating the upregulation of SphK1". Oncology Reports 36.2 (2016): 1016-1022.
Chicago
Fan, Z., Jiang, H., Wang, Z., Qu, J."Atorvastatin partially inhibits the epithelial-mesenchymal transition in A549 cells induced by TGF-β1 by attenuating the upregulation of SphK1". Oncology Reports 36, no. 2 (2016): 1016-1022. https://doi.org/10.3892/or.2016.4897
Copy and paste a formatted citation
x
Spandidos Publications style
Fan Z, Jiang H, Wang Z and Qu J: Atorvastatin partially inhibits the epithelial-mesenchymal transition in A549 cells induced by TGF-β1 by attenuating the upregulation of SphK1. Oncol Rep 36: 1016-1022, 2016.
APA
Fan, Z., Jiang, H., Wang, Z., & Qu, J. (2016). Atorvastatin partially inhibits the epithelial-mesenchymal transition in A549 cells induced by TGF-β1 by attenuating the upregulation of SphK1. Oncology Reports, 36, 1016-1022. https://doi.org/10.3892/or.2016.4897
MLA
Fan, Z., Jiang, H., Wang, Z., Qu, J."Atorvastatin partially inhibits the epithelial-mesenchymal transition in A549 cells induced by TGF-β1 by attenuating the upregulation of SphK1". Oncology Reports 36.2 (2016): 1016-1022.
Chicago
Fan, Z., Jiang, H., Wang, Z., Qu, J."Atorvastatin partially inhibits the epithelial-mesenchymal transition in A549 cells induced by TGF-β1 by attenuating the upregulation of SphK1". Oncology Reports 36, no. 2 (2016): 1016-1022. https://doi.org/10.3892/or.2016.4897
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