Effect of Epigallocatechin-3-Gallate on EGFR Signaling and Migration in Non-Small Cell Lung Cancer

The epidermal growth factor receptor (EGFR) is one of the most well-studied molecular targets in non-small cell lung cancer (NSCLC) and tyrosine kinase inhibitors have been shown to be effective in the treatment of advanced NSCLC. Nevertheless, the efficacy of tyrosine kinase inhibitors could be com...

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Autores principales:	Cristina Minnelli, Laura Cianfruglia, Emiliano Laudadio, Giovanna Mobbili, Roberta Galeazzi, Tatiana Armeni
Formato:	article
Lenguaje:	EN
Publicado:	MDPI AG 2021
Materias:	epigallocatechin-3-gallate (EGCG) epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) non-small cell lung cancer (NSCLC) Biology (General) QH301-705.5 Chemistry QD1-999
Acceso en línea:	https://doaj.org/article/cc12df14e2144e8fb730cf9ee4e75cc1
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spelling	oai:doaj.org-article:cc12df14e2144e8fb730cf9ee4e75cc12021-11-11T17:15:58ZEffect of Epigallocatechin-3-Gallate on EGFR Signaling and Migration in Non-Small Cell Lung Cancer10.3390/ijms2221118331422-00671661-6596https://doaj.org/article/cc12df14e2144e8fb730cf9ee4e75cc12021-10-01T00:00:00Zhttps://www.mdpi.com/1422-0067/22/21/11833https://doaj.org/toc/1661-6596https://doaj.org/toc/1422-0067The epidermal growth factor receptor (EGFR) is one of the most well-studied molecular targets in non-small cell lung cancer (NSCLC) and tyrosine kinase inhibitors have been shown to be effective in the treatment of advanced NSCLC. Nevertheless, the efficacy of tyrosine kinase inhibitors could be compromised by additional mutations in EGFR and compensatory activations of other pathways. Epigallocatechin-3-gallate (EGCG), the main bioactive molecule in green tea, acts as a tyrosine kinase inhibitor toward cancer cells overexpressing EGFR (wild-type). However, little information has been reported on the effect of EGCG on EGFR with activating mutations. In this study, we evaluated the ability of EGCG to inhibit EGFR signaling activation in three different NSCLC cell lines containing wild-type EGFR or EGFR with additional mutations. The effect on proliferation, apoptosis, migration, and vinculin expression was then studied. Overall, our results demonstrate that EGCG polyphenol inhibits cell proliferation and migration in NSCLC cell lines, although with different efficacy and mechanisms. These data may be of interest for an evaluation of the use of EGCG as an adjunct to NSCLC therapies.Cristina MinnelliLaura CianfrugliaEmiliano LaudadioGiovanna MobbiliRoberta GaleazziTatiana ArmeniMDPI AGarticleepigallocatechin-3-gallate (EGCG)epidermal growth factor receptor (EGFR)tyrosine kinase inhibitors (TKIs)non-small cell lung cancer (NSCLC)Biology (General)QH301-705.5ChemistryQD1-999ENInternational Journal of Molecular Sciences, Vol 22, Iss 11833, p 11833 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	epigallocatechin-3-gallate (EGCG) epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) non-small cell lung cancer (NSCLC) Biology (General) QH301-705.5 Chemistry QD1-999
spellingShingle	epigallocatechin-3-gallate (EGCG) epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) non-small cell lung cancer (NSCLC) Biology (General) QH301-705.5 Chemistry QD1-999 Cristina Minnelli Laura Cianfruglia Emiliano Laudadio Giovanna Mobbili Roberta Galeazzi Tatiana Armeni Effect of Epigallocatechin-3-Gallate on EGFR Signaling and Migration in Non-Small Cell Lung Cancer
description	The epidermal growth factor receptor (EGFR) is one of the most well-studied molecular targets in non-small cell lung cancer (NSCLC) and tyrosine kinase inhibitors have been shown to be effective in the treatment of advanced NSCLC. Nevertheless, the efficacy of tyrosine kinase inhibitors could be compromised by additional mutations in EGFR and compensatory activations of other pathways. Epigallocatechin-3-gallate (EGCG), the main bioactive molecule in green tea, acts as a tyrosine kinase inhibitor toward cancer cells overexpressing EGFR (wild-type). However, little information has been reported on the effect of EGCG on EGFR with activating mutations. In this study, we evaluated the ability of EGCG to inhibit EGFR signaling activation in three different NSCLC cell lines containing wild-type EGFR or EGFR with additional mutations. The effect on proliferation, apoptosis, migration, and vinculin expression was then studied. Overall, our results demonstrate that EGCG polyphenol inhibits cell proliferation and migration in NSCLC cell lines, although with different efficacy and mechanisms. These data may be of interest for an evaluation of the use of EGCG as an adjunct to NSCLC therapies.
format	article
author	Cristina Minnelli Laura Cianfruglia Emiliano Laudadio Giovanna Mobbili Roberta Galeazzi Tatiana Armeni
author_facet	Cristina Minnelli Laura Cianfruglia Emiliano Laudadio Giovanna Mobbili Roberta Galeazzi Tatiana Armeni
author_sort	Cristina Minnelli
title	Effect of Epigallocatechin-3-Gallate on EGFR Signaling and Migration in Non-Small Cell Lung Cancer
title_short	Effect of Epigallocatechin-3-Gallate on EGFR Signaling and Migration in Non-Small Cell Lung Cancer
title_full	Effect of Epigallocatechin-3-Gallate on EGFR Signaling and Migration in Non-Small Cell Lung Cancer
title_fullStr	Effect of Epigallocatechin-3-Gallate on EGFR Signaling and Migration in Non-Small Cell Lung Cancer
title_full_unstemmed	Effect of Epigallocatechin-3-Gallate on EGFR Signaling and Migration in Non-Small Cell Lung Cancer
title_sort	effect of epigallocatechin-3-gallate on egfr signaling and migration in non-small cell lung cancer
publisher	MDPI AG
publishDate	2021
url	https://doaj.org/article/cc12df14e2144e8fb730cf9ee4e75cc1
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Effect of Epigallocatechin-3-Gallate on EGFR Signaling and Migration in Non-Small Cell Lung Cancer

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