Evidence map›Paper›PMID 26168233›Full record

ArticleThe Journal of investigative dermatology2015

CCN2 Expression by Tumor Stroma Is Required for Melanoma Metastasis.

James Hutchenreuther, Krista M Vincent, David E Carter, Lynne-Marie Postovit, Andrew Leask

Abstract read
PubMed Publisher
In one paragraph

Article in The Journal of investigative dermatology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

25 citing papers in PubMed, 39 citations in OpenAlex.

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  19. Why target the tumor stroma in melanoma?Journal of cell communication and signaling · 2018
    Review
  20. Periostin in the pathogenesis of skin diseases.Cellular and molecular life sciences : CMLS · 2017
    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

5 authors at 2 institutions in 1 country.

James HutchenreutherDepartment of Physiology and Pharmacology and Dentistry, University of Western Ontario, London, Ontario, Canada.
Krista M VincentDepartment of Anatomy and Cell Biology, University of Western Ontario, London, Ontario, Canada.
David E CarterLondon Regional Genomics Centre, Robarts Institute, University of Western Ontario, London, Ontario, Canada.
Lynne-Marie PostovitDepartment of Anatomy and Cell Biology, University of Western Ontario, London, Ontario, Canada; Department of Oncology, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, Alberta, Canada.
Andrew LeaskDepartment of Physiology and Pharmacology and Dentistry, University of Western Ontario, London, Ontario, Canada. Electronic address: Andrew.leask@schulich.uwo.ca.
Western University · CAUniversity of Alberta · CA

Funding

Canadian Institutes of Health Research
6 · The paper itself

Abstract

Metastatic melanoma has an extremely poor prognosis with few durable remissions. The secreted matricellular protein connective tissue growth factor (CCN2) is overexpressed in cancers including melanoma and may represent a viable therapeutic target. However, the mechanism underlying the contribution of CCN2 to melanoma progression is unclear. Herein, we use the highly metastatic murine melanoma cell line B16(F10) and syngeneic mice, in which CCN2 expression is knocked out in fibroblasts, to demonstrate that loss of CCN2, either in melanoma cells or in the niche, impedes the ability of melanoma cells to invade. Specifically, loss of CCN2 in melanoma cells diminished their ability to invade through collagen in vitro, and loss of fibroblast-derived CCN2 decreased spontaneous metastases of melanoma cells from the skin to the lungs in vivo. Proliferation and tumor growth were not affected by loss of CCN2. CCN2-deficient B16(F10) cells showed reduced expression of the matricellular protein periostin; addition of recombinant periostin rescued the in vitro invasion defect of these cells. Immunohistochemical analysis of CCN2-deficient mice confirmed loss of periostin expression in the absence of CCN2. CCN2 and periostin mRNA levels are positively correlated with each other and with the stromal composition of human melanoma lesions but not BRAF mutations. Thus, CCN2 promotes invasion and metastasis via periostin and should be further evaluated as a possible therapeutic target for BRAF inhibitor-resistant melanoma.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsBiopsy, NeedleCell Line, TumorConnective Tissue Growth FactorDisease ProgressionFibroblastsHumansImmunohistochemistryMelanoma, ExperimentalMiceMice, Inbred C57BLMice, KnockoutNeoplasm MetastasisRNA, MessengerSkin NeoplasmsCCN2 protein, mouseConnective Tissue Growth FactorRNA, Messenger

Identifiers

PMID26168233
OpenAlexW1549495964

What OpenQuestion holds

Textmetadata
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.