LATS1 Is a Mediator of Melanogenesis in Response to Oxidative Stress and Regulator of Melanoma Growth

The LATS1 kinase has been described as a tumor suppressor in various cancers. However, its role in melanoma has not been fully elucidated. There are several processes involved in tumorigenesis, including melanin production. Melanin content positively correlates with the level of reactive oxygen spec...

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Main Authors: Urszula Kazimierczak, Ewelina Dondajewska, Maria Zajaczkowska, Marianna Karwacka, Tomasz Kolenda, Andrzej Mackiewicz
Format: Article
Language:English
Published: MDPI AG 2021-03-01
Series:International Journal of Molecular Sciences
Subjects:
Online Access:https://www.mdpi.com/1422-0067/22/6/3108
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spelling doaj-d417a36eb01c4129adf83b1d9cae32852021-03-19T00:02:27ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672021-03-01223108310810.3390/ijms22063108LATS1 Is a Mediator of Melanogenesis in Response to Oxidative Stress and Regulator of Melanoma GrowthUrszula Kazimierczak0Ewelina Dondajewska1Maria Zajaczkowska2Marianna Karwacka3Tomasz Kolenda4Andrzej Mackiewicz5Department of Cancer Immunology, Chair of Medical Biotechnology, Poznan University of Medical Sciences, Rokietnicka Street 8, 61-806 Poznan, PolandDepartment of Cancer Immunology, Chair of Medical Biotechnology, Poznan University of Medical Sciences, Rokietnicka Street 8, 61-806 Poznan, PolandDepartment of Cancer Immunology, Chair of Medical Biotechnology, Poznan University of Medical Sciences, Rokietnicka Street 8, 61-806 Poznan, PolandDepartment of Cancer Immunology, Chair of Medical Biotechnology, Poznan University of Medical Sciences, Rokietnicka Street 8, 61-806 Poznan, PolandDepartment of Cancer Immunology, Chair of Medical Biotechnology, Poznan University of Medical Sciences, Rokietnicka Street 8, 61-806 Poznan, PolandDepartment of Cancer Immunology, Chair of Medical Biotechnology, Poznan University of Medical Sciences, Rokietnicka Street 8, 61-806 Poznan, PolandThe LATS1 kinase has been described as a tumor suppressor in various cancers. However, its role in melanoma has not been fully elucidated. There are several processes involved in tumorigenesis, including melanin production. Melanin content positively correlates with the level of reactive oxygen species (ROS) inside the cell. Accordingly, the purpose of the study was to assess the role of LATS1 in melanogenesis and oxidative stress and its influence on tumor growth. We have knocked down LATS1 in primary melanocytes and melanoma cells and found that its expression is crucial for melanin synthesis, ROS production, and oxidative stress response. We showed that LATS1 ablation significantly decreased the melanogenesis markers’ expression and melanin synthesis in melanocyte and melanoma cell lines. Moreover, silencing LATS1 resulted in enhanced oxidative stress. Reduced melanin content in LATS1 knocked down tumors was associated with increased tumor growth, pointing to melanin’s protective role in this process. The study demonstrated that LATS1 is highly engaged in melanogenesis and oxidative stress control and affects melanoma growth. Our results may find the implications in the diagnosis and treatment of pigmentation disorders, including melanoma.https://www.mdpi.com/1422-0067/22/6/3108melanomaLATS1melanogenesisoxidative stress
collection DOAJ
language English
format Article
sources DOAJ
author Urszula Kazimierczak
Ewelina Dondajewska
Maria Zajaczkowska
Marianna Karwacka
Tomasz Kolenda
Andrzej Mackiewicz
spellingShingle Urszula Kazimierczak
Ewelina Dondajewska
Maria Zajaczkowska
Marianna Karwacka
Tomasz Kolenda
Andrzej Mackiewicz
LATS1 Is a Mediator of Melanogenesis in Response to Oxidative Stress and Regulator of Melanoma Growth
International Journal of Molecular Sciences
melanoma
LATS1
melanogenesis
oxidative stress
author_facet Urszula Kazimierczak
Ewelina Dondajewska
Maria Zajaczkowska
Marianna Karwacka
Tomasz Kolenda
Andrzej Mackiewicz
author_sort Urszula Kazimierczak
title LATS1 Is a Mediator of Melanogenesis in Response to Oxidative Stress and Regulator of Melanoma Growth
title_short LATS1 Is a Mediator of Melanogenesis in Response to Oxidative Stress and Regulator of Melanoma Growth
title_full LATS1 Is a Mediator of Melanogenesis in Response to Oxidative Stress and Regulator of Melanoma Growth
title_fullStr LATS1 Is a Mediator of Melanogenesis in Response to Oxidative Stress and Regulator of Melanoma Growth
title_full_unstemmed LATS1 Is a Mediator of Melanogenesis in Response to Oxidative Stress and Regulator of Melanoma Growth
title_sort lats1 is a mediator of melanogenesis in response to oxidative stress and regulator of melanoma growth
publisher MDPI AG
series International Journal of Molecular Sciences
issn 1661-6596
1422-0067
publishDate 2021-03-01
description The LATS1 kinase has been described as a tumor suppressor in various cancers. However, its role in melanoma has not been fully elucidated. There are several processes involved in tumorigenesis, including melanin production. Melanin content positively correlates with the level of reactive oxygen species (ROS) inside the cell. Accordingly, the purpose of the study was to assess the role of LATS1 in melanogenesis and oxidative stress and its influence on tumor growth. We have knocked down LATS1 in primary melanocytes and melanoma cells and found that its expression is crucial for melanin synthesis, ROS production, and oxidative stress response. We showed that LATS1 ablation significantly decreased the melanogenesis markers’ expression and melanin synthesis in melanocyte and melanoma cell lines. Moreover, silencing LATS1 resulted in enhanced oxidative stress. Reduced melanin content in LATS1 knocked down tumors was associated with increased tumor growth, pointing to melanin’s protective role in this process. The study demonstrated that LATS1 is highly engaged in melanogenesis and oxidative stress control and affects melanoma growth. Our results may find the implications in the diagnosis and treatment of pigmentation disorders, including melanoma.
topic melanoma
LATS1
melanogenesis
oxidative stress
url https://www.mdpi.com/1422-0067/22/6/3108
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