The TRPA1 Channel Amplifies the Oxidative Stress Signal in Melanoma

Macrophages (MΦs) and reactive oxygen species (ROS) are implicated in carcinogenesis. The oxidative stress sensor, transient receptor potential ankyrin 1 (TRPA1), activated by ROS, appears to contribute to lung and breast cancer progression. Although TRPA1 expression has been reported in melanoma ce...

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Autores principales:	Francesco De Logu, Daniel Souza Monteiro de Araujo, Filippo Ugolini, Luigi Francesco Iannone, Margherita Vannucchi, Francesca Portelli, Lorenzo Landini, Mustafa Titiz, Vincenzo De Giorgi, Pierangelo Geppetti, Daniela Massi, Romina Nassini
Formato:	article
Lenguaje:	EN
Publicado:	MDPI AG 2021
Materias:	oxidative stress melanoma macrophages TRPA1 image analysis Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/7eda8b07b7454584bffaea1e48d52eb5
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spelling	oai:doaj.org-article:7eda8b07b7454584bffaea1e48d52eb52021-11-25T17:11:48ZThe TRPA1 Channel Amplifies the Oxidative Stress Signal in Melanoma10.3390/cells101131312073-4409https://doaj.org/article/7eda8b07b7454584bffaea1e48d52eb52021-11-01T00:00:00Zhttps://www.mdpi.com/2073-4409/10/11/3131https://doaj.org/toc/2073-4409Macrophages (MΦs) and reactive oxygen species (ROS) are implicated in carcinogenesis. The oxidative stress sensor, transient receptor potential ankyrin 1 (TRPA1), activated by ROS, appears to contribute to lung and breast cancer progression. Although TRPA1 expression has been reported in melanoma cell lines, and oxidative stress has been associated with melanocytic transformation, their role in melanoma remains poorly known. Here, we localized MΦs, the final end-product of oxidative stress, 4-hydroxynonenal (4-HNE), and TRPA1 in tissue samples of human common dermal melanocytic nevi, dysplastic nevi, and thin (pT1) and thick (pT4) cutaneous melanomas. The number (amount) of intratumoral and peritumoral M2 MΦs and 4-HNE staining progressively increased with tumor severity, while TRPA1 expression was similar in all samples. Hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>) evoked a TRPA1-dependent calcium response in two distinct melanoma cell lines (SK-MEL-28 and WM266-4). Furthermore, H<sub>2</sub>O<sub>2</sub> induced a TRPA1-dependent H<sub>2</sub>O<sub>2</sub> release that was prevented by the TRPA1 antagonist, A967079, or <i>Trpa1</i> gene silencing (siRNA). ROS release from infiltrating M2 MΦs may target TRPA1-expressing melanoma cells to amplify the oxidative stress signal that affects tumor cell survival and proliferation.Francesco De LoguDaniel Souza Monteiro de AraujoFilippo UgoliniLuigi Francesco IannoneMargherita VannucchiFrancesca PortelliLorenzo LandiniMustafa TitizVincenzo De GiorgiPierangelo GeppettiDaniela MassiRomina NassiniMDPI AGarticleoxidative stressmelanomamacrophagesTRPA1image analysisBiology (General)QH301-705.5ENCells, Vol 10, Iss 3131, p 3131 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	oxidative stress melanoma macrophages TRPA1 image analysis Biology (General) QH301-705.5
spellingShingle	oxidative stress melanoma macrophages TRPA1 image analysis Biology (General) QH301-705.5 Francesco De Logu Daniel Souza Monteiro de Araujo Filippo Ugolini Luigi Francesco Iannone Margherita Vannucchi Francesca Portelli Lorenzo Landini Mustafa Titiz Vincenzo De Giorgi Pierangelo Geppetti Daniela Massi Romina Nassini The TRPA1 Channel Amplifies the Oxidative Stress Signal in Melanoma
description	Macrophages (MΦs) and reactive oxygen species (ROS) are implicated in carcinogenesis. The oxidative stress sensor, transient receptor potential ankyrin 1 (TRPA1), activated by ROS, appears to contribute to lung and breast cancer progression. Although TRPA1 expression has been reported in melanoma cell lines, and oxidative stress has been associated with melanocytic transformation, their role in melanoma remains poorly known. Here, we localized MΦs, the final end-product of oxidative stress, 4-hydroxynonenal (4-HNE), and TRPA1 in tissue samples of human common dermal melanocytic nevi, dysplastic nevi, and thin (pT1) and thick (pT4) cutaneous melanomas. The number (amount) of intratumoral and peritumoral M2 MΦs and 4-HNE staining progressively increased with tumor severity, while TRPA1 expression was similar in all samples. Hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>) evoked a TRPA1-dependent calcium response in two distinct melanoma cell lines (SK-MEL-28 and WM266-4). Furthermore, H<sub>2</sub>O<sub>2</sub> induced a TRPA1-dependent H<sub>2</sub>O<sub>2</sub> release that was prevented by the TRPA1 antagonist, A967079, or <i>Trpa1</i> gene silencing (siRNA). ROS release from infiltrating M2 MΦs may target TRPA1-expressing melanoma cells to amplify the oxidative stress signal that affects tumor cell survival and proliferation.
format	article
author	Francesco De Logu Daniel Souza Monteiro de Araujo Filippo Ugolini Luigi Francesco Iannone Margherita Vannucchi Francesca Portelli Lorenzo Landini Mustafa Titiz Vincenzo De Giorgi Pierangelo Geppetti Daniela Massi Romina Nassini
author_facet	Francesco De Logu Daniel Souza Monteiro de Araujo Filippo Ugolini Luigi Francesco Iannone Margherita Vannucchi Francesca Portelli Lorenzo Landini Mustafa Titiz Vincenzo De Giorgi Pierangelo Geppetti Daniela Massi Romina Nassini
author_sort	Francesco De Logu
title	The TRPA1 Channel Amplifies the Oxidative Stress Signal in Melanoma
title_short	The TRPA1 Channel Amplifies the Oxidative Stress Signal in Melanoma
title_full	The TRPA1 Channel Amplifies the Oxidative Stress Signal in Melanoma
title_fullStr	The TRPA1 Channel Amplifies the Oxidative Stress Signal in Melanoma
title_full_unstemmed	The TRPA1 Channel Amplifies the Oxidative Stress Signal in Melanoma
title_sort	trpa1 channel amplifies the oxidative stress signal in melanoma
publisher	MDPI AG
publishDate	2021
url	https://doaj.org/article/7eda8b07b7454584bffaea1e48d52eb5
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The TRPA1 Channel Amplifies the Oxidative Stress Signal in Melanoma

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