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10.3892/ol.2018.8963 http://scihub22266oqcxt.onion/10.3892/ol.2018.8963 C6036546!6036546 !30008942     free     free     free Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\30008942 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Oncol+Lett 2018 ; 16 (2 ): 2533-2538 Nephropedia Template TP {{tp|p=30008942 |t=2018. Overexpression of Napsin A resensitizes drug-resistant lung cancer A549 cells to gefitinib by inhibiting EMT |pdf=|usr=}}{{30008942 }} gab.com Text Overexpression of Napsin A resensitizes drug-resistant lung cancer A549 cells to gefitinib by inhibiting EMT JO: Oncol Lett http://www.kidney.de/pget.php?&tw=1&pmid=30008942 #FOAvip 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-overexpressing cells. Cell proliferation and apoptosis assays were performed to evaluate the effect of Napsin A overexpression on resistant A549 cells. The results of MTT assay demonstrated that Napsin A overexpression inhibited the proliferation of A549 and drug-resistant A549-GFT cells and that the proliferation of Napsin A-overexpressing A549-GFT cells was significantly inhibited by gefitinib treatment compared with control A549-GFT cells. The results from the Annexin V/propidium iodide double staining apoptosis assay indicated that Napsin A overexpression enhanced gefitinib-induced apoptosis in A549-GFT cells. Additionally, EMT was reversed following Napsin A expression in A549-GFT cells, as evidenced by the restoration of E-cadherin and downregulation of Vimentin expression. Further investigation demonstrated that Napsin A overexpression resulted in inhibition of focal adhesion kinase, a critical factor in integrin signaling, in the resistant A549-GFT cells. These data suggested that Napsin A resensitized the drug-resistant A549-GFT cells to gefitinib, possibly by reversing EMT via integrin signaling inhibition. Therefore, Napsin A combined with a TKI may be a more effective treatment strategy for lung cancer. Twit Text FOAVip Overexpression of Napsin A resensitizes drug-resistant lung cancer A549 cells to gefitinib by inhibiting EMT ????Oncol Lett http://www.kidney.de/pget.php?&tw=1&pmid=30008942 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=30008942 #FOAvip English Wikipedia <ref>{{Cite pmid|30008942 }}</ref> Overexpression of Napsin A resensitizes drug-resistant lung cancer A549 cells to gefitinib by inhibiting EMT #MMPMID30008942 Zhou L ; Lv X ; Yang J ; Zhu Y ; Wang Z ; Xu T Oncol Lett 2018[Aug]; 16 (2 ): 2533-2538 PMID30008942 show ga 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-overexpressing cells. Cell proliferation and apoptosis assays were performed to evaluate the effect of Napsin A overexpression on resistant A549 cells. The results of MTT assay demonstrated that Napsin A overexpression inhibited the proliferation of A549 and drug-resistant A549-GFT cells and that the proliferation of Napsin A-overexpressing A549-GFT cells was significantly inhibited by gefitinib treatment compared with control A549-GFT cells. The results from the Annexin V/propidium iodide double staining apoptosis assay indicated that Napsin A overexpression enhanced gefitinib-induced apoptosis in A549-GFT cells. Additionally, EMT was reversed following Napsin A expression in A549-GFT cells, as evidenced by the restoration of E-cadherin and downregulation of Vimentin expression. Further investigation demonstrated that Napsin A overexpression resulted in inhibition of focal adhesion kinase, a critical factor in integrin signaling, in the resistant A549-GFT cells. These data suggested that Napsin A resensitized the drug-resistant A549-GFT cells to gefitinib, possibly by reversing EMT via integrin signaling inhibition. Therefore, Napsin A combined with a TKI may be a more effective treatment strategy for lung cancer. äOverexpression of Napsin A resensitizes drug-resistant lung cancer A54(epmc).pdf DeepDyve Pubget Overpricing