Evidence map›Paper›PMID 26918341›Full record

ArticleOncotarget2016

Gene expression analyses of primary melanomas reveal CTHRC1 as an important player in melanoma progression.

Johanna Eriksson, Vadim Le Joncour, Pirjo Nummela, Tiina Jahkola, Susanna Virolainen, Pirjo Laakkonen, Olli Saksela, Erkki Hölttä

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 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

36 citing papers in PubMed, 71 citations in OpenAlex.

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  10. Leveraging gene correlations in single cell transcriptomic data.bioRxiv : the preprint server for biology · 2023
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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 2 institutions in 1 country.

Johanna ErikssonDepartment of Pathology, University of Helsinki, FI-00014 Helsinki, Finland.
Vadim Le JoncourUniversity of Helsinki, Research Programs Unit, Translational Cancer Biology, Biomedicum Helsinki, FI-00014 Helsinki, Finland.
Pirjo NummelaDepartment of Pathology, University of Helsinki, FI-00014 Helsinki, Finland.
Tiina JahkolaDepartment of Plastic Surgery, Helsinki University Central Hospital, FI-00029 Helsinki, Finland.
Susanna VirolainenDepartment of Pathology, University of Helsinki, FI-00014 Helsinki, Finland.
Pirjo LaakkonenUniversity of Helsinki, Research Programs Unit, Translational Cancer Biology, Biomedicum Helsinki, FI-00014 Helsinki, Finland.
Olli SakselaDepartment of Dermatology, Helsinki University Central Hospital, FI-00029 Helsinki, Finland.
Erkki HölttäDepartment of Pathology, University of Helsinki, FI-00014 Helsinki, Finland.
University of Helsinki · FIHelsinki University Hospital · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Melanoma is notorious for its high tendency to metastasize and its refractoriness to conventional treatments after metastasis, and the responses to most targeted therapies are short-lived. A better understanding of the molecular mechanisms behind melanoma development and progression is needed to develop more effective therapies and to identify new markers to predict disease behavior. Here, we compared the gene expression profiles of benign nevi, and non-metastatic and metastatic primary melanomas to identify any common changes in disease progression. We identified several genes associated with inflammation, angiogenesis, and extracellular matrix modification to be upregulated in metastatic melanomas. We selected one of these genes, collagen triple helix repeat containing 1 (CTHRC1), for detailed analysis, and found that CTHRC1 was expressed in both melanoma cells and the associated fibroblasts, as well as in the endothelium of tumor blood vessels. Knockdown of CTHRC1 expression by shRNAs in melanoma cells inhibited their migration in Transwell assays and their invasion in three-dimensional collagen and Matrigel matrices. We also elucidated the possible down-stream effectors of CTHRC1 by gene expression profiling of the CTHRC1-knockdown cells. Our analyses showed that CTHRC1 is regulated coordinately with fibronectin and integrin β3 by the pro-invasive and -angiogenic transcription factor NFATC2. We also found CTHRC1 to be a target of TFGβ and BRAF. These data highlight the importance of tumor stroma in melanoma progression. Furthermore, CTHRC1 was recognized as an important mediator of melanoma cell migration and invasion, providing together with its regulators-NFATC2, TGFβ, and BRAF-attractive therapeutic targets against metastatic melanomas.

Indexed as

Gene Expression ProfilingGene Expression Regulation, NeoplasticAnimalsApoptosisBiomarkers, TumorCell AdhesionCell MovementCell ProliferationCutaneous Malignant MelanomaDisease ProgressionExtracellular Matrix ProteinsFemaleFibronectinsHumansIntegrin beta3MelanocytesBiomarkers, TumorCTHRC1 protein, humanExtracellular Matrix ProteinsFibronectinsFN1 protein, humanIntegrin beta3ITGB3 protein, humanNFATC2 protein, humanNFATC Transcription FactorsCTHRC1invasion/metastasismelanomaNFATC2TGFβ

Identifiers

PMID26918341
PMCPMC4924771
OpenAlexW2297912038

What Socratic 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 Socratic graph.