EGFR-L858R mutant enhances lung adenocarcinoma cell invasive ability and promotes malignant pleural effusion formation through activation of the CXCL12-CXCR4 pathway

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題名:	EGFR-L858R mutant enhances lung adenocarcinoma cell invasive ability and promotes malignant pleural effusion formation through activation of the CXCL12-CXCR4 pathway
作者:	許藝瓊;Tsai, Meng-Feng;Chang, Tzu-Hua;Wu, Shang-Gin;Yang, Hsiao-Yin;Hsu, Yi-Chiung;Yang, Pan-Chyr;Shih, Jin-Yuan
貢獻者:	生醫理工學院生醫科學與工程學系
關鍵詞:	631/67/1612/1350;631/80/86;Adenocarcinoma;Adenocarcinoma - genetics;Adenocarcinoma - metabolism;Adenocarcinoma - pathology;Cell Line, Tumor;Chemokine CXCL12 - metabolism;CXCL12 protein;CXCR4 protein;Ectopic expression;Epidermal growth factor;Epidermal growth factor receptors;Humanities and Social Sciences;Humans;Invasiveness;Lung cancer;Lung carcinoma;Lung Neoplasms - genetics;Lung Neoplasms - metabolism;Lung Neoplasms - pathology;Molecular modelling;multidisciplinary;Mutation;Mutation - genetics;Neoplasm Invasiveness;Non-small cell lung carcinoma;Pleural cavity;Pleural effusion;Pleural Effusion, Malignant - genetics;Pleural Effusion, Malignant - metabolism;Pleural Effusion, Malignant - pathology;Receptor, Epidermal Growth Factor - genetics;Receptors, CXCR4 - metabolism;Science;Signal Transduction;siRNA;Small cell lung carcinoma
日期:	2015-09-04
上傳時間:	2026-04-23 11:15:50 (UTC+8)
出版者:	Nature Publishing Group;London: Springer Science and Business Media LLC
摘要:	摘要： AbstractMalignant pleural effusion (MPE) is a common clinical problem in non-small cell lung carcinoma (NSCLC) patients; however, the underlying mechanisms are still largely unknown. Recent studies indicate that the frequency of the L858R mutant form of the epidermal growth factor receptor (EGFR-L858R) is higher in lung adenocarcinoma with MPE than in surgically resected specimens, suggesting that lung adenocarcinoma cells harboring this mutation tend to invade the adjacent pleural cavity. The purpose of this study was to clarify the relationship between the EGFR-L858R mutation and cancer cell invasion ability and to investigate the molecular mechanisms involved in the formation of MPE. We found that expression of EGFR-L858R in lung cancer cells resulted in up-regulation of the CXCR4 in association with increased cancer cell invasive ability and MPE formation. Ectopic expression of EGFR-L858R in lung cancer cells acted through activation of ERK signaling pathways to induce the expression of CXCR4. We also indicated that Inhibition of CXCR4 with small interfering RNA, neutralizing antibody, or receptor antagonist significantly suppressed the EGFR-L858R–dependent cell invasion. These results suggest that targeting the production of CXCR4 and blocking the CXCL12-CXCR4 pathway might be effective strategies for treating NSCLCs harboring a specific type of EGFR mutation. 其他題名： Sci Rep 出版者： London: Springer Science and Business Media LLC 出版日期： 2015-09-04 出處： Scientific Reports, 2015-09, Vol.5 (1), p.13574-13574, Article 13574 資源來源： Publicly Available Content Database (Proquest) 版權： The Author(s) 2015 版權： Copyright Nature Publishing Group Sep 2015 版權： Copyright © 2015, Macmillan Publishers Limited 2015 Macmillan Publishers Limited 識別號： ISSN: 2045-2322 識別號： EISSN: 2045-2322 識別號： DOI: 10.1038/srep13574 識別號： PMID: 26338423
顯示於類別:	[生醫科學與工程學系] 期刊論文

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