Evidence map›Paper›PMID 23973372›Full record

ArticleMolecular cell2013

MC1R is a potent regulator of PTEN after UV exposure in melanocytes.

Juxiang Cao, Lixin Wan, Elke Hacker, Xiangpeng Dai, Stefania Lenna, Celia Jimenez-Cervantes, Yongjun Wang, Nick R Leslie, George X Xu, Hans R Widlund and 7 more

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cell, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed
7.3field-weighted citation impact, top 2% 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

79 citing papers in PubMed, 141 citations in OpenAlex.

  1. Trial
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  5. An overview of benefits and risks of chronic melanocortin-1 receptor activation.Journal of the European Academy of Dermatology and Venereology : JEADV · 2025
    Review
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19 more citing papers are in PubMed but not listed here.

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

17 authors at 10 institutions in 5 countries.

Juxiang CaoDepartment of Dermatology, Boston University School of Medicine, 609 Albany Street, Boston, MA 02118, USA.
Lixin Wan
Elke Hacker
Xiangpeng Dai
Stefania Lenna
Celia Jimenez-Cervantes
Yongjun Wang
Nick R Leslie
George X Xu
Hans R Widlund
Byungwoo Ryu
Rhoda M Alani
Ken Dutton-Regester
Colin R Goding
Nicholas K Hayward
Wenyi Wei
Rutao Cui
Boston University · USBeth Israel Deaconess Medical Center · USQIMR Berghofer Medical Research Institute · AUBrigham and Women's Hospital · USHeriot-Watt University · GBQueensland University of Technology · AUShanghai University of Traditional Chinese Medicine · CNUniversidad de Murcia · ESUniversity of Oxford · GBUniversity of Pennsylvania · US

Funding

Boston University Clinical and Translational Science Award (CTSA) Program UL1UL1TR000157 · NCATS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI CENTER, DAVID M. · 2012 to 2013
$7.9M
Interplay between Cdh1 and major regulatory pathways in human cancerR01GM089763 · NIGMS · BETH ISRAEL DEACONESS MEDICAL CENTER · PI WEI, WENYI · 2009 to 2018
$3.0M
The role of pheomelanin in cutaneous melanomaR01CA137098 · NCI · TUFTS MEDICAL CENTER · PI CUI, RUTAO · 2009 to 2014
$1.6M
Functional analysis of beta-TRCP in cell cycle control and DNA damage responseR01GM094777 · NIGMS · BETH ISRAEL DEACONESS MEDICAL CENTER · PI WEI, WENYI · 2012 to 2015
$1.3M
Medical Research Council G0801865NCATS NIH HHS UL1 TR000157NCATS NIH HHS UL1-TR000157NCI NIH HHS 1R01CA137098NCI NIH HHS R01 CA137098NIGMS NIH HHS GM089763NIGMS NIH HHS R01 GM089763NIGMS NIH HHS R01 GM094777
6 · The paper itself

Abstract

The individuals carrying melanocortin-1 receptor (MC1R) variants, especially those associated with red hair color, fair skin, and poor tanning ability (RHC trait), are more prone to melanoma; however, the underlying mechanism is poorly defined. Here, we report that UVB exposure triggers phosphatase and tensin homolog (PTEN) interaction with wild-type (WT), but not RHC-associated MC1R variants, which protects PTEN from WWP2-mediated degradation, leading to AKT inactivation. Strikingly, the biological consequences of the failure of MC1R variants to suppress PI3K/AKT signaling are highly context dependent. In primary melanocytes, hyperactivation of PI3K/AKT signaling leads to premature senescence; in the presence of BRAF(V600E), MC1R deficiency-induced elevated PI3K/AKT signaling drives oncogenic transformation. These studies establish the MC1R-PTEN axis as a central regulator for melanocytes' response to UVB exposure and reveal the molecular basis underlying the association between MC1R variants and melanomagenesis.

Indexed as

Ultraviolet Raysalpha-MSHAnimalsBlotting, WesternCells, CulturedGene Expression RegulationHumansImmunoenzyme TechniquesMelanocytesMelanoma, ExperimentalMiceMutationPhosphatidylinositol 3-KinasesPhosphorylationProto-Oncogene Proteins B-rafProto-Oncogene Proteins c-aktalpha-MSHBRAF protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins B-rafProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePTEN protein, humanReceptor, Melanocortin, Type 1RNA, Messenger

Identifiers

PMID23973372
PMCPMC3792490
OpenAlexW2036262371

What OpenQuestion holds

Textmetadata
LicenceTDM
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.