Next Article in Journal
Energy Metabolism Plays a Critical Role in Stem Cell Maintenance and Differentiation
Next Article in Special Issue
Oncostatic-Cytoprotective Effect of Melatonin and Other Bioactive Molecules: A Common Target in Mitochondrial Respiration
Previous Article in Journal
Antinociceptive and Anti-Inflammatory Effects of Zerumbone against Mono-Iodoacetate-Induced Arthritis
Previous Article in Special Issue
The Metabolic Fate of ortho-Quinones Derived from Catecholamine Metabolites
Open AccessArticle

Hinokitiol Inhibits Melanogenesis via AKT/mTOR Signaling in B16F10 Mouse Melanoma Cells

Division of Nephrology, Department of Medicine, Taoyuan General Hospital, Taoyuan 330, Taiwan
Institute of Clinical Medicine, National Yang-Ming University, Taipei 11221, Taiwan
Department of Microbiology, School of Medicine, China Medical University, Taichung 404, Taiwan
Graduate Institute of Basic Medical Science, School of Medicine, China Medical University, Taichung 404, Taiwan
Department of Environmental Engineering and Science, Feng Chia University, Taichung 40407, Taiwan
Department of Biological Sciences, National Sun Yat-sen University, Kaohsiung 804, Taiwan
Author to whom correspondence should be addressed.
Academic Editor: Manickam Sugumaran
Int. J. Mol. Sci. 2016, 17(2), 248;
Received: 14 January 2016 / Revised: 4 February 2016 / Accepted: 15 February 2016 / Published: 18 February 2016
(This article belongs to the Special Issue Biochemistry and Mechanisms of Melanogenesis)
H inokitiol purified from the heartwood of cupressaceous plants has had various biological functions of cell differentiation and growth. Hinokitiol has been demonstrated as having an important role in anti-inflammation and anti-bacteria effect, suggesting that it is potentially useful in therapies for hyperpigmentation. Previously, hinokitiol inhibited the production of melanin by inhibiting tyrosinase activity. The autophagic signaling pathway can induce hypopigmentation. This study is warranted to investigate the mechanism of hinokitiol-induced hypopigmentation through autophagy in B16F10 melanoma cells. The melanin contents and expression of microthphalmia associated transcription factor (MITF) and tyrosinase were inhibited by treatment with hinokitiol. Moreover, the phosphorylation of the protein express levels of phospho-protein kinase B (P-AKT) and phospho-mammalian targets of rapamycin (P-mTOR) were reduced after hinokitiol treatment. In addition, the microtubule associated protein 1 light chain 3 (LC3) -II and beclin 1 (autophagic markers) were increased after the B16F10 cell was treated with hinokitiol. Meanwhile, hinokitiol decreased cellular melanin contents in a dose-dependent manner. These findings establish that hinokitiol inhibited melanogenesis through the AKT/mTOR signaling pathway. View Full-Text
Keywords: hinokitiol; melanogenesis; autophagy; melanoma hinokitiol; melanogenesis; autophagy; melanoma
Show Figures

Graphical abstract

MDPI and ACS Style

Tsao, Y.-T.; Huang, Y.-F.; Kuo, C.-Y.; Lin, Y.-C.; Chiang, W.-C.; Wang, W.-K.; Hsu, C.-W.; Lee, C.-H. Hinokitiol Inhibits Melanogenesis via AKT/mTOR Signaling in B16F10 Mouse Melanoma Cells. Int. J. Mol. Sci. 2016, 17, 248.

Show more citation formats Show less citations formats
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

Search more from Scilit
Back to TopTop