Evidence map›Paper›PMID 30457212›Full record

ArticlePigment cell & melanoma research2019

The lncRNA RMEL3 protects immortalized cells from serum withdrawal-induced growth arrest and promotes melanoma cell proliferation and tumor growth.

Cibele Cardoso, Rodolfo B Serafim, Akinori Kawakami, Cristiano Gonçalves Pereira, Jason Roszik, Valeria Valente, Vinicius L Vazquez, David E Fisher, Enilza M Espreafico

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in Pigment cell & melanoma research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.9field-weighted citation impact, top 31% 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

13 citing papers in PubMed, 26 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 4 institutions in 2 countries.

Cibele CardosoDepartment of Cell and Molecular Biology, Faculty of Medicine of Ribeirão Preto, University of São Paulo, Ribeirão Preto, Brazil.
Rodolfo B SerafimDepartment of Cell and Molecular Biology, Faculty of Medicine of Ribeirão Preto, University of São Paulo, Ribeirão Preto, Brazil.
Akinori KawakamiCutaneous Biology Research Center, Department of Dermatology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts.
Cristiano Gonçalves PereiraDepartment of Cell and Molecular Biology, Faculty of Medicine of Ribeirão Preto, University of São Paulo, Ribeirão Preto, Brazil.
Jason RoszikDepartment of Melanoma Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Valeria ValenteDepartment of Cell and Molecular Biology, Faculty of Medicine of Ribeirão Preto, University of São Paulo, Ribeirão Preto, Brazil.
Vinicius L VazquezMolecular Oncology Research Center (CPOM) and Melanoma/Sarcoma Surgery Department, Barretos Cancer Hospital, Barretos, Brazil.
David E FisherCutaneous Biology Research Center, Department of Dermatology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts.ORCID 0000-0002-5506-0575
Enilza M EspreaficoDepartment of Cell and Molecular Biology, Faculty of Medicine of Ribeirão Preto, University of São Paulo, Ribeirão Preto, Brazil.ORCID 0000-0002-7552-4234
Universidade de São Paulo · BRHarvard University · USHospital de Câncer de Barretos · BRThe University of Texas MD Anderson Cancer Center · US

Funding

Transcriptional mechanisms and melanomaP01CA163222 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI DAVID E FISHER · 2013 to 2026
$25.3M
The MITF transcriptional network: melanoma risk and carcinogenesisR01AR043369 · NIAMS · MASSACHUSETTS GENERAL HOSPITAL · PI DAVID E FISHER · 1996 to 2026
$9.4M
Therapeutic strategies for treatment of giant congenital melanocytic neviR01AR072304 · NIAMS · MASSACHUSETTS GENERAL HOSPITAL · PI DAVID E FISHER · 2017 to 2026
$3.9M
A druggable dependency in low-MITF/high-AXL melanoma: preclinical efficacy and mechanism of action in a key treatment-resistant subclass.R01CA222871 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI FISHER, DAVID E · 2018 to 2022
$1.8M
Conselho Nacional de Desenvolvimento Científico e Tecnológico 309187/2015-0Conselho Nacional de Desenvolvimento Científico e Tecnológico 457603/2013-5Conselho Nacional de Desenvolvimento Científico e Tecnológico 465687/2014-8Conselho Nacional de Desenvolvimento Científico e Tecnológico 870310/1997-6Fundação de Amparo à Pesquisa do Estado de São Paulo 2010/16097-5Fundação de Amparo à Pesquisa do Estado de São Paulo 2012/24056-2Fundação de Amparo à Pesquisa do Estado de São Paulo 2013/08135-2Fundação de Amparo à Pesquisa do Estado de São Paulo 2013/13465-1Fundação de Amparo à Pesquisa do Estado de São Paulo 2014/18189-5Fundação de Amparo à Pesquisa do Estado de São Paulo 2014/50928-2Fundação de Amparo à Pesquisa do Estado de São Paulo 2018/04017-9NCI NIH HHS P01 CA163222NCI NIH HHS R01 CA222871NIAMS NIH HHS R01 AR043369NIAMS NIH HHS R01 AR072304
6 · The paper itself

Abstract

RMEL3 is a recently identified lncRNA associated with BRAFV600E mutation and melanoma cell survival. Here, we demonstrate strong and moderate RMEL3 upregulation in BRAF and NRAS mutant melanoma cells, respectively, compared to melanocytes. High expression is also more frequent in cutaneous than in acral/mucosal melanomas, and analysis of an ICGC melanoma dataset showed that mutations in RMEL3 locus are preponderantly C > T substitutions at dipyrimidine sites including CC > TT, typical of UV signature. RMEL3 mutation does not correlate with RMEL3 levels, but does with poor patient survival, in TCGA melanoma dataset. Accordingly, RMEL3 lncRNA levels were significantly reduced in BRAFV600E melanoma cells upon treatment with BRAF or MEK inhibitors, supporting the notion that BRAF-MEK-ERK pathway plays a role to activate RMEL3 gene transcription. RMEL3 overexpression, in immortalized fibroblasts and melanoma cells, increased proliferation and survival under serum starvation, clonogenic ability, and xenografted melanoma tumor growth. Although future studies will be needed to elucidate the mechanistic activities of RMEL3, our data demonstrate that its overexpression bypasses the need of mitogen activation to sustain proliferation/survival of non-transformed cells and suggest an oncogenic role for RMEL3.

Indexed as

CytoprotectionAnimalsApoptosisCarcinogenesisCell Line, TransformedCell Line, TumorCell ProliferationClone CellsFibroblastsGene Expression Regulation, NeoplasticGTP PhosphohydrolasesHumansMelanomaMembrane ProteinsMiceMitogen-Activated Protein KinasesGTP PhosphohydrolasesMembrane ProteinsMitogen-Activated Protein KinasesNRAS protein, humanProtein Kinase InhibitorsProto-Oncogene Proteins B-rafRNA, Long NoncodingBRAFV600Echr5:57395060-57533424 (GRCh38/hg38)CTD-2023N9.1ENSG00000250961.1LncGPBP1-1:1MAPKmelanomamitogenserum response

Identifiers

PMID30457212
PMCPMC6613776
OpenAlexW2901133680

What OpenQuestion holds

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Registered trials

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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.