ArticleOncology letters2021
Lentivirus-mediated silencing of CNTN1 enhances gefitinib sensitivity by reversing epithelial-mesenchymal transition in lung adenocarcinoma A549 cells.
Article in Oncology letters, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- PFKM Promotes the Progression of Gastric Cancer by Up-regulating CNTN1 Expression Through H3K18la Modification.Applied biochemistry and biotechnology · 2025Article
- PI3K/AKT pathway as a pivotal regulator of epithelial-mesenchymal transition in lung tumor cells.Cancer cell international · 2024Review
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7 authors.
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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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