Open Access

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

  • Published online on: March 31, 2021     https://doi.org/10.3892/ol.2021.12694
  • Article Number: 433
  • Copyright: © Hu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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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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June-2021
Volume 21 Issue 6

Print ISSN: 1792-1074
Online ISSN:1792-1082

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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