Overcoming epithelial-mesenchymal transition-mediated drug resistance with monensin-based combined therapy in non-small cell lung cancer
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Abstract
Background</br> The epithelial-mesenchymal transition (EMT) is a key process in tumor progression and metastasis and is also associated with drug resistance. Thus, controlling EMT status is a research of interest to conquer the malignant tumors.</br> Materials and methods</br> A drug repositioning analysis of transcriptomic data from a public cell line database identified monensin, a widely used in veterinary medicine, as a candidate EMT inhibitor that suppresses the conversion of the EMT phenotype. Using TGF-β-induced EMT cell line models, the effects of monensin on the EMT status and EMT-mediated drug resistance were assessed.</br> Results</br> TGF-β treatment induced EMT in non-small cell lung cancer (NSCLC) cell lines and the EGFR-mutant NSCLC cell lines with TGF-β-induced EMT acquired resistance to EGFR-tyrosine kinase inhibitor. The addition of monensin effectively suppressed the TGF-β-induced-EMT conversion, and restored the growth inhibition and the induction of apoptosis by the EGFR-tyrosine kinase inhibitor.</br> Conclusion</br> Our data suggested that combined therapy with monensin might be a useful strategy for preventing EMT-mediated acquired drug resistance.
Journal
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- Biochemical and Biophysical Research Communications
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Biochemical and Biophysical Research Communications 529 (3), 760-765, 2020-08-27
Academic Press
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Keywords
Details 詳細情報について
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- CRID
- 1050288834686116096
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- NII Article ID
- 120007120054
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- NII Book ID
- AA00564395
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- ISSN
- 0006291X
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- Text Lang
- en
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- Article Type
- journal article
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- Data Source
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- IRDB
- Crossref
- CiNii Articles
- KAKEN