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Lentivirus‑mediated silencing of CNTN1 enhances gefitinib sensitivity by reversing epithelial‑mesenchymal transition in lung adenocarcinoma A549 cells

  • Authors:
    • Chun-Sheng Hu
    • Jiu-Hong Huang
    • Dong-Lin Yang
    • Chuan Xu
    • Zhi-Gang Xu
    • Hong-Bo Tan
    • Zhong-Zhu Chen
  • View Affiliations / Copyright

    Affiliations: College of Pharmacy, National and Local Joint Engineering Research Center of Targeted and Innovative Therapeutics, Chongqing Key Laboratory of Kinase Modulators as Innovative Medicine, Chongqing University of Arts and Sciences, Chongqing 402160, P.R. China, Department of Oncology, Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan 610047, P.R. China
    Copyright: © Hu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 433
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    Published online on: March 31, 2021
       https://doi.org/10.3892/ol.2021.12694
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Abstract

Contactin‑1 (CNTN1), a neuronal cell adhesion molecular, functions in nervous system development and has been associated with carcinogenesis and tumor progression. To investigate the role of CNTN1 in gefitinib resistance in lung adenocarcinoma, lentivirus‑mediated short hairpin (sh)RNA was used to silence CNTN1 and its physiological function was analyzed in the A549 cell line. A cell cytotoxicity assay revealed that CNTN1 knockdown enhanced gefitinib sensitivity in the A549 cells. In addition, CNTN1 knockdown, together with gefitinib treatment, resulted in a significant inhibition of colony formation and migration, and promotion of apoptosis. Furthermore, CNTN1 knockdown also reversed the epithelial‑mesenchymal transition (EMT) phenotype by increasing E‑cadherin protein expression level, and decreasing N‑cadherin and vimentin protein expression levels. The PI3K/Akt signaling pathway was also association with the effects of CNTN1 on EMT progression and gefitinib resistance in the A549 cells. Collectively, knockdown of CNTN1 reversed the EMT phenotype and enhanced gefitinib sensitivity in the A549 cells by inhibiting the activation of the PI3K/Akt signaling pathway. These results suggested that CNTN1 may represent a potential therapeutic target for reserving EGFR‑tyrosine kinase inhibitor resistance in non‑small cell lung cancer.
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Copy and paste a formatted citation
Spandidos Publications style
Hu C, Huang J, Yang D, Xu C, Xu Z, Tan H and Chen Z: Lentivirus‑mediated silencing of CNTN1 enhances gefitinib sensitivity by reversing epithelial‑mesenchymal transition in lung adenocarcinoma A549 cells. Oncol Lett 21: 433, 2021.
APA
Hu, C., Huang, J., Yang, D., Xu, C., Xu, Z., Tan, H., & Chen, Z. (2021). Lentivirus‑mediated silencing of CNTN1 enhances gefitinib sensitivity by reversing epithelial‑mesenchymal transition in lung adenocarcinoma A549 cells. Oncology Letters, 21, 433. https://doi.org/10.3892/ol.2021.12694
MLA
Hu, C., Huang, J., Yang, D., Xu, C., Xu, Z., Tan, H., Chen, Z."Lentivirus‑mediated silencing of CNTN1 enhances gefitinib sensitivity by reversing epithelial‑mesenchymal transition in lung adenocarcinoma A549 cells". Oncology Letters 21.6 (2021): 433.
Chicago
Hu, C., Huang, J., Yang, D., Xu, C., Xu, Z., Tan, H., Chen, Z."Lentivirus‑mediated silencing of CNTN1 enhances gefitinib sensitivity by reversing epithelial‑mesenchymal transition in lung adenocarcinoma A549 cells". Oncology Letters 21, no. 6 (2021): 433. https://doi.org/10.3892/ol.2021.12694
Copy and paste a formatted citation
x
Spandidos Publications style
Hu C, Huang J, Yang D, Xu C, Xu Z, Tan H and Chen Z: Lentivirus‑mediated silencing of CNTN1 enhances gefitinib sensitivity by reversing epithelial‑mesenchymal transition in lung adenocarcinoma A549 cells. Oncol Lett 21: 433, 2021.
APA
Hu, C., Huang, J., Yang, D., Xu, C., Xu, Z., Tan, H., & Chen, Z. (2021). Lentivirus‑mediated silencing of CNTN1 enhances gefitinib sensitivity by reversing epithelial‑mesenchymal transition in lung adenocarcinoma A549 cells. Oncology Letters, 21, 433. https://doi.org/10.3892/ol.2021.12694
MLA
Hu, C., Huang, J., Yang, D., Xu, C., Xu, Z., Tan, H., Chen, Z."Lentivirus‑mediated silencing of CNTN1 enhances gefitinib sensitivity by reversing epithelial‑mesenchymal transition in lung adenocarcinoma A549 cells". Oncology Letters 21.6 (2021): 433.
Chicago
Hu, C., Huang, J., Yang, D., Xu, C., Xu, Z., Tan, H., Chen, Z."Lentivirus‑mediated silencing of CNTN1 enhances gefitinib sensitivity by reversing epithelial‑mesenchymal transition in lung adenocarcinoma A549 cells". Oncology Letters 21, no. 6 (2021): 433. https://doi.org/10.3892/ol.2021.12694
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