Evidence map›Paper›PMID 36080217›Full record

ArticleMolecules (Basel, Switzerland)2022

BCI-215, a Dual-Specificity Phosphatase Inhibitor, Reduces UVB-Induced Pigmentation in Human Skin by Activating Mitogen-Activated Protein Kinase Pathways.

Jeong Hyeon Lee, Myoung Eun Choi, Hongchan An, Ju Won Moon, Hye Jin Yeo, Youngsup Song, Sung Eun Chang

Open access · goldAbstract read
In one paragraph

Article in Molecules (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.1field-weighted citation impact, top 59% 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

3 citing papers in PubMed, 2 citations in OpenAlex.

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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

7 authors at 2 institutions in 1 country.

Jeong Hyeon LeeDepartment of Biomedical Sciences, Bio-Medical Institute of Technology (BMIT), University of Ulsan College of Medicine, Ulsan 44610, Korea.
Myoung Eun ChoiDepartment of Dermatology, Asan Medical Institute of Convergence Science and Technology, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, Korea.ORCID 0000-0001-7514-7873
Hongchan AnNew Drug Development Center, Daegu-Gyeongbuk Medical Innovation Foundation, Daegu 41061, Korea.ORCID 0000-0001-6689-9571
Ju Won MoonDepartment of Biomedical Sciences, Bio-Medical Institute of Technology (BMIT), University of Ulsan College of Medicine, Ulsan 44610, Korea.ORCID 0000-0002-1451-389X
Hye Jin YeoDepartment of Biomedical Sciences, Bio-Medical Institute of Technology (BMIT), University of Ulsan College of Medicine, Ulsan 44610, Korea.
Youngsup SongDepartment of Biomedical Sciences, University of Ulsan College of Medicine, Asan Institute for Life Sciences, Asan Medical Center, Seoul 05505, Korea.ORCID 0000-0002-6268-5223
Sung Eun ChangDepartment of Dermatology, Asan Medical Institute of Convergence Science and Technology, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, Korea.
Ulsan College · KRDaegu-Gyeongbuk Medical Innovation Foundation · KR

Funding

National Research Foundation of Korea 2020R1A4A4079708
6 · The paper itself

Abstract

backgroundThe dysregulation of melanin production causes skin-disfiguring ultraviolet (UV)-associated hyperpigmented spots. Previously, we found that the activation of c-Jun N-terminal kinase (JNK), a mitogen-activated protein kinase (MAPK), inhibited melanogenesis.

methodsWe selected BCI-215 as it may modify MAPK expression via a known function of a dual-specificity phosphatase (DUSP) 1/6 inhibitor. B16F10 melanoma cells, Mel-ab cells, human melanocytes, and a coculture were used to assess the anti-melanogenic activity of BCI-215. The molecular mechanisms were deciphered by assaying the melanin content and cellular tyrosinase activity via immunoblotting and RT-PCR.

resultsBCI-215 was found to suppress basal and cAMP-stimulated melanin production and cellular tyrosinase activity in vitro through the downregulation of microphthalmia-associated transcription factor (MITF) protein and its downstream enzymes. The reduction in MITF expression caused by BCI-215 was found to be due to all three types of MAPK activation, including extracellular signal-regulated kinase (ERK), JNK, and p38. The degree of activation was greater in ERK. A phosphorylation of the β-catenin pathway was also demonstrated. The melanin index, expression of MITF, and downstream enzymes were well-reduced in UVB-irradiated ex vivo human skin by BCI-215.

conclusionsAs BCI-215 potently inhibits UV-stimulated melanogenesis, small molecules of DUSP-related signaling modulators may provide therapeutic benefits against pigmentation disorders.

Indexed as

Brain-Computer InterfacesDual-Specificity PhosphatasesHyperpigmentationCell Line, TumorExtracellular Signal-Regulated MAP KinasesHumansMelaninsMelanocytesMonophenol MonooxygenasePigmentationDual-Specificity PhosphatasesExtracellular Signal-Regulated MAP KinasesMelaninsMonophenol MonooxygenaseBCI-215dual-specificity phosphatasemelanogenesismitogen-activated protein kinaseultraviolet radiation

Identifiers

PMID36080217
PMCPMC9458123
OpenAlexW4293206999

What OpenQuestion holds

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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.