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Article

The TRPA1 Channel Amplifies the Oxidative Stress Signal in Melanoma

1
Department of Health Sciences, Clinical Pharmacology and Oncology Section, University of Florence, 50139 Florence, Italy
2
Advanced Bioimaging Research Laboratory (ABiR), University of Florence, 50139 Florence, Italy
3
Research Unit ChrOnic PAin Laboratory (CoPAL), University of Florence, 50139 Florence, Italy
4
Department of Health Sciences, Section of Pathological Anatomy, University of Florence, 50139 Florence, Italy
5
Headache Center and Clinical Pharmacology, Careggi University Hospital, 50139 Florence, Italy
6
Division of Dermatology, Azienda Sanitaria Firenze, 50139 Florence, Italy
*
Author to whom correspondence should be addressed.
Academic Editors: Lin-Hua Jiang, Xiaoqiang Yao and Bilal Çiğ
Cells 2021, 10(11), 3131; https://doi.org/10.3390/cells10113131
Received: 15 October 2021 / Revised: 9 November 2021 / Accepted: 9 November 2021 / Published: 11 November 2021
(This article belongs to the Special Issue TRP Channels in Oxidative Stress Signalling)
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 (H2O2) evoked a TRPA1-dependent calcium response in two distinct melanoma cell lines (SK-MEL-28 and WM266-4). Furthermore, H2O2 induced a TRPA1-dependent H2O2 release that was prevented by the TRPA1 antagonist, A967079, or Trpa1 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. View Full-Text
Keywords: oxidative stress; melanoma; macrophages; TRPA1; image analysis oxidative stress; melanoma; macrophages; TRPA1; image analysis
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MDPI and ACS Style

De Logu, F.; Souza Monteiro de Araujo, D.; Ugolini, F.; Iannone, L.F.; Vannucchi, M.; Portelli, F.; Landini, L.; Titiz, M.; De Giorgi, V.; Geppetti, P.; Massi, D.; Nassini, R. The TRPA1 Channel Amplifies the Oxidative Stress Signal in Melanoma. Cells 2021, 10, 3131. https://doi.org/10.3390/cells10113131

AMA Style

De Logu F, Souza Monteiro de Araujo D, Ugolini F, Iannone LF, Vannucchi M, Portelli F, Landini L, Titiz M, De Giorgi V, Geppetti P, Massi D, Nassini R. The TRPA1 Channel Amplifies the Oxidative Stress Signal in Melanoma. Cells. 2021; 10(11):3131. https://doi.org/10.3390/cells10113131

Chicago/Turabian Style

De Logu, Francesco, Daniel Souza Monteiro de Araujo, Filippo Ugolini, Luigi F. Iannone, Margherita Vannucchi, Francesca Portelli, Lorenzo Landini, Mustafa Titiz, Vincenzo De Giorgi, Pierangelo Geppetti, Daniela Massi, and Romina Nassini. 2021. "The TRPA1 Channel Amplifies the Oxidative Stress Signal in Melanoma" Cells 10, no. 11: 3131. https://doi.org/10.3390/cells10113131

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