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MicroRNA-7 enhances cytotoxicity induced by gefitinib in non-small cell lung cancer via inhibiting the EGFR and IGF1R signalling pathways

Gefitinib is a tyrosine kinase inhibitor that has been used for the treatment of non-small-cell lung carcinoma (NSCLC). The ability of miR-7 to enhance gefitinib-induced cytotoxicity in NSCLC cells was evaluated in this study. We found that miR-7 significantly decreased the IC50 of gefitinib and inh...

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Detalles Bibliográficos
Autores principales: Zhao, Jun-gang, Men, Wan-fu, Tang, Jun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Termedia Publishing House 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4631286/
https://www.ncbi.nlm.nih.gov/pubmed/26557760
http://dx.doi.org/10.5114/wo.2015.52655
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author Zhao, Jun-gang
Men, Wan-fu
Tang, Jun
author_facet Zhao, Jun-gang
Men, Wan-fu
Tang, Jun
author_sort Zhao, Jun-gang
collection PubMed
description Gefitinib is a tyrosine kinase inhibitor that has been used for the treatment of non-small-cell lung carcinoma (NSCLC). The ability of miR-7 to enhance gefitinib-induced cytotoxicity in NSCLC cells was evaluated in this study. We found that miR-7 significantly decreased the IC50 of gefitinib and inhibited cell growth. G0/G1 cell cycle arrest and cell apoptosis were increased after the treatment of gefitinib coupled with miR-7 transfection. In addition, levels of Raf1, IGF1R, and PI3K and phosphorylation levels of Akt and ERK were also significantly decreased. Our results suggest that miR-7 may provide a novel therapeutic target for the treatment of NSCLCs.
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spelling pubmed-46312862015-11-10 MicroRNA-7 enhances cytotoxicity induced by gefitinib in non-small cell lung cancer via inhibiting the EGFR and IGF1R signalling pathways Zhao, Jun-gang Men, Wan-fu Tang, Jun Contemp Oncol (Pozn) Original Paper Gefitinib is a tyrosine kinase inhibitor that has been used for the treatment of non-small-cell lung carcinoma (NSCLC). The ability of miR-7 to enhance gefitinib-induced cytotoxicity in NSCLC cells was evaluated in this study. We found that miR-7 significantly decreased the IC50 of gefitinib and inhibited cell growth. G0/G1 cell cycle arrest and cell apoptosis were increased after the treatment of gefitinib coupled with miR-7 transfection. In addition, levels of Raf1, IGF1R, and PI3K and phosphorylation levels of Akt and ERK were also significantly decreased. Our results suggest that miR-7 may provide a novel therapeutic target for the treatment of NSCLCs. Termedia Publishing House 2015-07-08 2015 /pmc/articles/PMC4631286/ /pubmed/26557760 http://dx.doi.org/10.5114/wo.2015.52655 Text en Copyright © 2015 Termedia http://creativecommons.org/licenses/by-nc-nd/3.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution-Noncommercial 3.0 Unported License, permitting all non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Paper
Zhao, Jun-gang
Men, Wan-fu
Tang, Jun
MicroRNA-7 enhances cytotoxicity induced by gefitinib in non-small cell lung cancer via inhibiting the EGFR and IGF1R signalling pathways
title MicroRNA-7 enhances cytotoxicity induced by gefitinib in non-small cell lung cancer via inhibiting the EGFR and IGF1R signalling pathways
title_full MicroRNA-7 enhances cytotoxicity induced by gefitinib in non-small cell lung cancer via inhibiting the EGFR and IGF1R signalling pathways
title_fullStr MicroRNA-7 enhances cytotoxicity induced by gefitinib in non-small cell lung cancer via inhibiting the EGFR and IGF1R signalling pathways
title_full_unstemmed MicroRNA-7 enhances cytotoxicity induced by gefitinib in non-small cell lung cancer via inhibiting the EGFR and IGF1R signalling pathways
title_short MicroRNA-7 enhances cytotoxicity induced by gefitinib in non-small cell lung cancer via inhibiting the EGFR and IGF1R signalling pathways
title_sort microrna-7 enhances cytotoxicity induced by gefitinib in non-small cell lung cancer via inhibiting the egfr and igf1r signalling pathways
topic Original Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4631286/
https://www.ncbi.nlm.nih.gov/pubmed/26557760
http://dx.doi.org/10.5114/wo.2015.52655
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