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Benzo(a)pyrene enhances the EMT-associated migration of lung adenocarcinoma A549 cells by upregulating Twist1

  • Authors:
    • Xi Chen
    • Hongbing Peng
    • Jian Xiao
    • Anqi Guan
    • Bin Xie
    • Bixiu He
    • Qiong Chen
  • View Affiliations / Copyright

    Affiliations: Department of Respiratory Medicine, Xiangya Hospital of Central South University, Changsha, Hunan 410008, P.R. China, Department of Geriatrics, Respiratory Medicine, Xiangya Hospital of Central South University, Changsha, Hunan 410008, P.R. China
    Copyright: © Chen et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 2141-2147
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    Published online on: August 3, 2017
       https://doi.org/10.3892/or.2017.5874
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Abstract

Benzo(a)pyrene (BaP), an important toxic component of cigarette smoke, can cause lung cancer and lead to the progression of lung cancer. In the present study, we investigated the effect of BaP on the migration of lung adenocarcinoma A549 cells. BaP (1 µM) promoted the migration of A549 cells in a time-dependent manner and upregulated the expression of the Twist family BHLH transcription factor 1 (Twist1). BaP also induced upregulation of the mesenchymal markers N-cadherin and vimentin and downregulation of the epithelial marker E-cadherin. When the expression of Twist1 was knocked down in A549 cells that were treated with BaP for 4 weeks (A549BaP-4w), the expression of Twist1 decreased, which inhibited the migration capacity of A549BaP-4w cells, the expression of N-cadherin and vimentin was downregulated and the expression of E-cadherin was upregulated. In addition, morphological observations of A549BaP-4w cells revealed that the epithelial characteristics of A549 cells became mesenchymal characteristics. When the expression of Twist1 was knocked down, the A549BaP-4w cells were transformed back to cells with epithelial characteristics. In conclusion, the results from the present study indicate that BaP enhances the epithelial-mesenchymal transition-associated migration of lung adenocarcinoma A549 cells by upregulating Twist1.
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Copy and paste a formatted citation
Spandidos Publications style
Chen X, Peng H, Xiao J, Guan A, Xie B, He B and Chen Q: Benzo(a)pyrene enhances the EMT-associated migration of lung adenocarcinoma A549 cells by upregulating Twist1. Oncol Rep 38: 2141-2147, 2017.
APA
Chen, X., Peng, H., Xiao, J., Guan, A., Xie, B., He, B., & Chen, Q. (2017). Benzo(a)pyrene enhances the EMT-associated migration of lung adenocarcinoma A549 cells by upregulating Twist1. Oncology Reports, 38, 2141-2147. https://doi.org/10.3892/or.2017.5874
MLA
Chen, X., Peng, H., Xiao, J., Guan, A., Xie, B., He, B., Chen, Q."Benzo(a)pyrene enhances the EMT-associated migration of lung adenocarcinoma A549 cells by upregulating Twist1". Oncology Reports 38.4 (2017): 2141-2147.
Chicago
Chen, X., Peng, H., Xiao, J., Guan, A., Xie, B., He, B., Chen, Q."Benzo(a)pyrene enhances the EMT-associated migration of lung adenocarcinoma A549 cells by upregulating Twist1". Oncology Reports 38, no. 4 (2017): 2141-2147. https://doi.org/10.3892/or.2017.5874
Copy and paste a formatted citation
x
Spandidos Publications style
Chen X, Peng H, Xiao J, Guan A, Xie B, He B and Chen Q: Benzo(a)pyrene enhances the EMT-associated migration of lung adenocarcinoma A549 cells by upregulating Twist1. Oncol Rep 38: 2141-2147, 2017.
APA
Chen, X., Peng, H., Xiao, J., Guan, A., Xie, B., He, B., & Chen, Q. (2017). Benzo(a)pyrene enhances the EMT-associated migration of lung adenocarcinoma A549 cells by upregulating Twist1. Oncology Reports, 38, 2141-2147. https://doi.org/10.3892/or.2017.5874
MLA
Chen, X., Peng, H., Xiao, J., Guan, A., Xie, B., He, B., Chen, Q."Benzo(a)pyrene enhances the EMT-associated migration of lung adenocarcinoma A549 cells by upregulating Twist1". Oncology Reports 38.4 (2017): 2141-2147.
Chicago
Chen, X., Peng, H., Xiao, J., Guan, A., Xie, B., He, B., Chen, Q."Benzo(a)pyrene enhances the EMT-associated migration of lung adenocarcinoma A549 cells by upregulating Twist1". Oncology Reports 38, no. 4 (2017): 2141-2147. https://doi.org/10.3892/or.2017.5874
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