Melatonin exerts oncostatic capacity and decreases melanogenesis in human MNT-1 melanoma cells.

electron paramagnetic resonance spectroscopy liquid chromatography-mass spectroscopy melanogenesis melanoma cells melatonin transmission electron microscopy tyrosinase activity

Journal

Journal of pineal research
ISSN: 1600-079X
Titre abrégé: J Pineal Res
Pays: England
ID NLM: 8504412

Informations de publication

Date de publication:
Nov 2019
Historique:
received: 10 05 2019
revised: 23 08 2019
accepted: 09 09 2019
pubmed: 19 9 2019
medline: 13 3 2020
entrez: 19 9 2019
Statut: ppublish

Résumé

Melanogenesis is a key parameter of differentiation in melanocytes and melanoma cells; therefore, search for factors regulating this pathway are strongly desired. Herein, we investigated the effects of melatonin, a ubiquitous physiological mediator that is found throughout animals and plants. In mammals, the pineal gland secretes this indoleamine into the blood circulation to exert an extensive repertoire of biological activities. Our in vitro assessment indicates an oncostatic capacity of melatonin in time-dependent manner (24, 48, 72 hours) in highly pigmented MNT-1 melanoma cells. The similar pattern of regulation regarding cell viability was observed in amelanotic Sk-Mel-28 cells. Subsequently, MNT-1 cells were tested for the first time for evaluation of melanin/melatonin interaction. Thus primary, electron paramagnetic resonance (EPR) spectroscopy demonstrated that melatonin reduced melanin content. Artificially induced disturbances of melanogenesis by selected inhibitors (N-phenylthiourea or kojic acid) were slightly antagonized by melatonin. Additionally, analysis using transmission electron microscopy has shown that melatonin, particularly at higher dose of 10

Identifiants

pubmed: 31532834
doi: 10.1111/jpi.12610
pmc: PMC7924888
mid: NIHMS1671821
doi:

Substances chimiques

Melanins 0
Melatonin JL5DK93RCL

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

e12610

Subventions

Organisme : NIH Clinical Center
ID : 1R01AR073004-01A1
Organisme : NIH Clinical Center
ID : 1R01AR056666-01A2
Organisme : NIAMS NIH HHS
ID : R01 AR073004
Pays : United States
Organisme : NIH Clinical Center
ID : 1RO1AR071189-01A1
Organisme : Narodowe Centrum Nauki
ID : Sonata-2015/19/D/ST4/01964
Organisme : NIAMS NIH HHS
ID : R01 AR071189
Pays : United States
Organisme : Deutsche Forschungsgemeinschaft (DFG)
ID : KL2900/2-1
Organisme : NIAMS NIH HHS
ID : R01 AR056666
Pays : United States

Informations de copyright

© 2019 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

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Auteurs

Konrad Kleszczyński (K)

Department of Dermatology, University of Münster, Münster, Germany.

Tae-Kang Kim (TK)

Department of Dermatology, Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL, USA.

Bernadetta Bilska (B)

Department of Cell Biology and Imaging, Institute of Zoology and Biomedical Research, Jagiellonian University, Kraków, Poland.

Michal Sarna (M)

Department of Biophysics, Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University, Kraków, Poland.

Krystian Mokrzynski (K)

Department of Biophysics, Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University, Kraków, Poland.

Agatha Stegemann (A)

Department of Dermatology, University of Münster, Münster, Germany.

Elżbieta Pyza (E)

Department of Cell Biology and Imaging, Institute of Zoology and Biomedical Research, Jagiellonian University, Kraków, Poland.

Russel J Reiter (RJ)

Department of Cellular and Structural Biology, UT Health, San Antonio, TX, USA.

Kerstin Steinbrink (K)

Department of Dermatology, University of Münster, Münster, Germany.

Markus Böhm (M)

Department of Dermatology, University of Münster, Münster, Germany.

Andrzej T Slominski (AT)

Department of Dermatology, Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL, USA.
Pathology and Laboratory Medicine Service, VA Medical Center, Birmingham, AL, USA.

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