Evidence map›Paper›PMID 26135897›Full record

ArticleBritish journal of cancer2015

Overexpression of connexin 43 reduces melanoma proliferative and metastatic capacity.

A Tittarelli, I Guerrero, F Tempio, M A Gleisner, I Avalos, S Sabanegh, C Ortíz, L Michea, M N López, A Mendoza-Naranjo and 1 more

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2015. 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 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

39 citing papers in PubMed, 71 citations in OpenAlex.

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  4. Injury-induced connexin 43 expression regulates endothelial wound healing.American journal of physiology. Heart and circulatory physiology · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 2 institutions in 2 countries.

A TittarelliInstitute of Biomedical Sciences, Faculty of Medicine, University of Chile, Santiago 8380453, Chile.
I GuerreroInstitute of Biomedical Sciences, Faculty of Medicine, University of Chile, Santiago 8380453, Chile.
F Tempio1] Institute of Biomedical Sciences, Faculty of Medicine, University of Chile, Santiago 8380453, Chile [2] Millennium Institute on Immunology and Immunotherapy, Institute of Biomedical Sciences, University of Chile, Santiago 8380453, Chile.
M A GleisnerInstitute of Biomedical Sciences, Faculty of Medicine, University of Chile, Santiago 8380453, Chile.
I AvalosInstitute of Biomedical Sciences, Faculty of Medicine, University of Chile, Santiago 8380453, Chile.
S SabaneghInstitute of Biomedical Sciences, Faculty of Medicine, University of Chile, Santiago 8380453, Chile.
C OrtízInstitute of Biomedical Sciences, Faculty of Medicine, University of Chile, Santiago 8380453, Chile.
L Michea1] Institute of Biomedical Sciences, Faculty of Medicine, University of Chile, Santiago 8380453, Chile [2] Millennium Institute on Immunology and Immunotherapy, Institute of Biomedical Sciences, University of Chile, Santiago 8380453, Chile.
M N López1] Institute of Biomedical Sciences, Faculty of Medicine, University of Chile, Santiago 8380453, Chile [2] Millennium Institute on Immunology and Immunotherapy, Institute of Biomedical Sciences, University of Chile, Santiago 8380453, Chile [3] Research Support Office, University of Chile Clinical Hospital, Santiago 8380453, Chile.
A Mendoza-NaranjoUCL Cancer Institute, University College London, 72 Huntley Street, London WC1E 6DD, UK.
F Salazar-Onfray1] Institute of Biomedical Sciences, Faculty of Medicine, University of Chile, Santiago 8380453, Chile [2] Millennium Institute on Immunology and Immunotherapy, Institute of Biomedical Sciences, University of Chile, Santiago 8380453, Chile.
University of Chile · CLUniversity College London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAlterations in connexin 43 (Cx43) expression and/or gap junction (GJ)-mediated intercellular communication are implicated in cancer pathogenesis. Herein, we have investigated the role of Cx43 in melanoma cell proliferation and apoptosis sensitivity in vitro, as well as metastatic capability and tumour growth in vivo.

methodsConnexin 43 expression levels, GJ coupling and proliferation rates were analysed in four different human melanoma cell lines. Furthermore, tumour growth and lung metastasis of high compared with low Cx43-expressing FMS cells were evaluated in vivo using a melanoma xenograft model.

resultsSpecific inhibition of Cx43 channel activity accelerated melanoma cell proliferation, whereas overexpression of Cx43 increased GJ coupling and reduced cell growth. Moreover, Cx43 overexpression in FMS cells increased basal and tumour necrosis factor-α-induced apoptosis and resulted in decreased melanoma tumour growth and lower number and size of metastatic foci in vivo.

conclusionsOur findings reveal an important role for Cx43 in intrinsically controlling melanoma growth, death and metastasis, and emphasise the potential use of compounds that selectively enhance Cx43 expression on melanoma in the future chemotherapy and/or immunotherapy protocols.

Indexed as

Cell ProliferationAnimalsApoptosisCalciumCell CommunicationCell Line, TumorConnexin 43Gap JunctionsHumansMelanomaMiceMice, Inbred NODNeoplasm MetastasisCalciumConnexin 43

Identifiers

PMID26135897
PMCPMC4506378
OpenAlexW1937228880

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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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.