Overexpression of Napsin A resensitizes drug-resistant lung cancer A549 cells to gefitinib by inhibiting EMT

Oncology Letters
Linshui ZhouTingzhen Xu

Abstract

Lung cancer is one of the most common malignant tumors and also the leading cause of cancer-related deaths in the world. Epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKI), such as gefitinib, have been used in the therapy of lung cancer. However, the acquisition of drug resistance is a major limitation in the clinical efficiency of EGFR-TKIs. Epithelial-mesenchymal transition (EMT) has been demonstrated to be an underlying mechanism of acquired resistance. A previous study has reported that Napsin A expression can inhibit EMT in lung cancer cells. The present study therefore investigated the effect of Napsin A on the sensitivity of EGFR-TKI-resistant lung cancer cells. First, a drug-resistant lung cancer cell line was generated using the EGFR-TKI gefitinib on A549 cells (termed here A549-GFT). EMT was demonstrated to be induced in the drug resistant A549-GFT cells, evidenced by reduced E-cadherin expression and increased Vimentin expression compared with control A549 cells. Next, Napsin A was overexpressed in the cells by transfection of the Napsin A-expression vector, PLJM1-Napsin A. Western blot analysis confirmed that the protein expression levels of Napsin A were significantly elevated in the Napsin A-ov...Continue Reading

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Citations

Jul 15, 2021·Pathology Oncology Research : POR·Sören WeidemannSarah Minner

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