Evidence map›Paper›PMID 27206672›Full record

ArticleOncotarget2016

Reprogramming human A375 amelanotic melanoma cells by catalase overexpression: Reversion or promotion of malignancy by inducing melanogenesis or metastasis.

Candelaria Bracalente, Noelia Salguero, Cintia Notcovich, Carolina B Müller, Leonardo L da Motta, Fabio Klamt, Irene L Ibañez, Hebe Durán

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

8 citing papers in PubMed, 16 citations in OpenAlex.

  1. Targeting catalase in cancer.Redox biology · 2024
    Review
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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 4 institutions in 2 countries.

Candelaria BracalenteDepartamento de Micro y Nanotecnología, Comisión Nacional de Energía Atómica, San Martín, Buenos Aires, B1650KNA, Argentina.
Noelia SalgueroDepartamento de Micro y Nanotecnología, Comisión Nacional de Energía Atómica, San Martín, Buenos Aires, B1650KNA, Argentina.
Cintia NotcovichDepartamento de Micro y Nanotecnología, Comisión Nacional de Energía Atómica, San Martín, Buenos Aires, B1650KNA, Argentina.
Carolina B MüllerLaboratório de Bioquímica Celular, Departamento de Bioquímica, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Porto Alegre, 90035 003, Brasil.
Leonardo L da MottaLaboratório de Bioquímica Celular, Departamento de Bioquímica, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Porto Alegre, 90035 003, Brasil.
Fabio KlamtLaboratório de Bioquímica Celular, Departamento de Bioquímica, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Porto Alegre, 90035 003, Brasil.
Irene L IbañezDepartamento de Micro y Nanotecnología, Comisión Nacional de Energía Atómica, San Martín, Buenos Aires, B1650KNA, Argentina.
Hebe DuránDepartamento de Micro y Nanotecnología, Comisión Nacional de Energía Atómica, San Martín, Buenos Aires, B1650KNA, Argentina.
Comisión Nacional de Energía Atómica · ARUniversidade Federal do Rio Grande do Sul · BRCentro Científico Tecnológico - San Juan · ARNational University of General San Martín · AR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Advanced melanoma is the most aggressive form of skin cancer. It is highly metastatic and dysfunctional in melanogenesis; two processes that are induced by H2O2. This work presents a melanoma cell model with low levels of H2O2 induced by catalase overexpression to study differentiation/dedifferentiation processes. Three clones (A7, C10 and G10) of human A375 amelanotic melanoma cells with quite distinct phenotypes were obtained. These clones faced H2O2 scavenging by two main strategies. One developed by clone G10 where ROS increased. This resulted in G10 migration and metastasis associated with the increased of cofilin-1 and CAP1. The other strategy was observed in clone A7 and C10, where ROS levels were maintained reversing malignant features. Particularly, C10 was not tumorigenic, while A7 reversed the amelanotic phenotype by increasing melanin content and melanocytic differentiation markers. These clones allowed the study of potential differentiation and migration markers and its association with ROS levels in vitro and in vivo, providing a new melanoma model with different degree of malignancy.

Indexed as

AnimalsCatalaseCell DedifferentiationCell DifferentiationCell Line, TumorCell Transformation, NeoplasticCellular ReprogrammingClone CellsFemaleGene Expression Regulation, NeoplasticHumansHydrogen PeroxideMelaninsMelanoma, AmelanoticMiceMice, NudeCatalaseHydrogen PeroxideMelaninscatalasemelanogenesis and metastasismelanomaROS

Identifiers

PMID27206672
PMCPMC5173048
OpenAlexW2402589183

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.