Evidence map›Paper›PMID 26293674›Full record

ArticleOncotarget2015

Glucose transporter isoform 1 expression enhances metastasis of malignant melanoma cells.

Andreas Koch, Sven Arke Lang, Peter Johannes Wild, Susanne Gantner, Abdo Mahli, Gerrit Spanier, Mark Berneburg, Martina Müller, Anja Katrin Bosserhoff, Claus Hellerbrand

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
4.2field-weighted citation impact, top 4% 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

55 citing papers in PubMed, 91 citations in OpenAlex.

  1. Article
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  14. Insulin and cancer: a tangled web.The Biochemical journal · 2022
    Review
  15. Article
  16. Connecting Metabolic Rewiring With Phenotype Switching in Melanoma.Frontiers in cell and developmental biology · 2022
    Review
  17. Review
  18. Article
  19. Article
  20. Review
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

10 authors at 3 institutions in 2 countries.

Andreas KochDepartment of Internal Medicine I, University Hospital Regensburg, Germany.
Sven Arke LangDepartment of Surgery, University Hospital Regensburg, Germany.
Peter Johannes WildInstitute of Pathology, University Hospital Zurich, Switzerland.
Susanne GantnerDepartment of Dermatology, University Hospital Regensburg, Germany.
Abdo MahliDepartment of Internal Medicine I, University Hospital Regensburg, Germany.
Gerrit SpanierDepartment of Cranio-Maxillo-Facial Surgery, University Hospital Regensburg, Germany.
Mark BerneburgDepartment of Dermatology, University Hospital Regensburg, Germany.
Martina MüllerDepartment of Internal Medicine I, University Hospital Regensburg, Germany.
Anja Katrin BosserhoffInstitute of Biochemistry, University of Erlangen, Germany.
Claus HellerbrandDepartment of Internal Medicine I, University Hospital Regensburg, Germany.
University Hospital Regensburg · DEFriedrich-Alexander-Universität Erlangen-Nürnberg · DEUniversity Hospital of Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The glucose transporter isoform 1 (GLUT1; SLC2A1) is a key rate-limiting factor in the transport of glucose into cancer cells. Enhanced GLUT1 expression and accelerated glycolysis have been found to promote aggressive growth in a range of tumor entities. However, it was unknown whether GLUT1 directly impacts metastasis. Here, we aimed at analyzing the expression and function of GLUT1 in malignant melanoma. Immunohistochemical analysis of 78 primary human melanomas on a tissue micro array showed that GLUT1 expression significantly correlated with the mitotic activity and a poor survival. To determine the functional role of GLUT1 in melanoma, we stably suppressed GLUT1 in the murine melanoma cell line B16 with shRNA. GLUT1 suppressed melanoma cells revealed significantly reduced proliferation, apoptosis resistance, migratory activity and matrix metalloproteinase 2 (MMP2) expression. In a syngeneic murine model of hepatic metastasis, GLUT1-suppressed cells formed significantly less metastases and showed increased apoptosis compared to metastases formed by control cells. Treatment of four different human melanoma cell lines with a pharmacological GLUT1 inhibitor caused a dose-dependent reduction of proliferation, apoptosis resistance, migratory activity and MMP2 expression. Analysis of MAPK signal pathways showed that GLUT1 inhibition significantly decreased JNK activation, which regulates a wide range of targets in the metastatic cascade. In summary, our study provides functional evidence that enhanced GLUT1 expression in melanoma cells favors their metastatic behavior. These findings specify GLUT1 as an attractive therapeutic target and prognostic marker for this highly aggressive tumor.

Indexed as

Cell MovementAntineoplastic AgentsApoptosisCell Line, TumorCell ProliferationDose-Response Relationship, DrugFemaleGene Expression Regulation, NeoplasticGlucose Transporter Type 1HumansHydroxybenzoatesImmunohistochemistryJNK Mitogen-Activated Protein KinasesKaplan-Meier EstimateLiver NeoplasmsMaleAntineoplastic AgentsGlucose Transporter Type 1HydroxybenzoatesJNK Mitogen-Activated Protein KinasesMatrix Metalloproteinase 2Mmp2 protein, mouseSLC2A1 protein, humanSlc2a1 protein, mouseWZB117GLUT1glycolysisJNKmelanomametastasis

Identifiers

PMID26293674
PMCPMC4741727
OpenAlexW2126410297

What OpenQuestion holds

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LicenceCC BY
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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.