Evidence map›Paper›PMID 26901194›Full record

ArticleInternational journal of molecular sciences2016

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

Yu-Tzu Tsao, Yu-Fen Huang, Chun-Yu Kuo, Yu-Chiang Lin, Wei-Cheng Chiang, Wei-Kuang Wang, Chia-Wei Hsu, Che-Hsin Lee

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
4.0field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 42 citations in OpenAlex.

  1. Regulatory effects ofInternational journal of medical sciences · 2021
    Trial
  2. Unraveling the Antimelanogenic Potential ofJournal of agricultural and food chemistry · 2026
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  13. The extracts ofInternational journal of medical sciences · 2020
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 1 country.

Yu-Tzu TsaoDivision of Nephrology, Department of Medicine, Taoyuan General Hospital, Taoyuan 330, Taiwan. tsaoyutzu@gmail.com.
Yu-Fen HuangDepartment of Microbiology, School of Medicine, China Medical University, Taichung 404, Taiwan. u103000425@cmu.edu.tw.
Chun-Yu KuoGraduate Institute of Basic Medical Science, School of Medicine, China Medical University, Taichung 404, Taiwan. u104082801@cmu.edu.tw.
Yu-Chiang LinGraduate Institute of Basic Medical Science, School of Medicine, China Medical University, Taichung 404, Taiwan. s225701048@gmail.com.
Wei-Cheng ChiangDepartment of Environmental Engineering and Science, Feng Chia University, Taichung 40407, Taiwan. winton05@hotmail.com.
Wei-Kuang WangDepartment of Environmental Engineering and Science, Feng Chia University, Taichung 40407, Taiwan. wkwang@fcu.edu.tw.
Chia-Wei HsuGraduate Institute of Basic Medical Science, School of Medicine, China Medical University, Taichung 404, Taiwan. m5210115@gmail.com.
Che-Hsin LeeDepartment of Microbiology, School of Medicine, China Medical University, Taichung 404, Taiwan. chlee@mail.cmu.edu.tw.
China Medical University · TWFeng Chia University · TWTao Yuan General Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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.

Indexed as

AnimalsAntineoplastic Agents, PhytogenicCell Line, TumorMelaninsMelanoma, ExperimentalMiceMicrophthalmia-Associated Transcription FactorMonophenol MonooxygenaseMonoterpenesPhosphorylationProto-Oncogene Proteins c-aktSignal TransductionTOR Serine-Threonine KinasesTropoloneAntineoplastic Agents, Phytogenicbeta-thujaplicinMelaninsMicrophthalmia-Associated Transcription FactorMonophenol MonooxygenaseMonoterpenesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesTropoloneautophagyhinokitiolmelanogenesismelanoma

Identifiers

PMID26901194
PMCPMC4783978
OpenAlexW2275402822

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.