Evidence map›Paper›PMID 33087801›Full record

ArticleScientific reports2020

Identification of drivers of breast cancer invasion by secretome analysis: insight into CTGF signaling.

Johanna W Hellinger, Franziska Schömel, Judith V Buse, Christof Lenz, Gerd Bauerschmitz, Günter Emons, Carsten Gründker

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 22% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.

  1. Pooled it
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  13. Cancer secretome: finding out hidden messages in extracellular secretions.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 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

7 authors at 1 institution in 1 country.

Johanna W HellingerDepartment of Gynecology and Obstetrics, University Medicine Göttingen, Robert-Koch-Str. 40, 37075, Göttingen, Germany.
Franziska SchömelDepartment of Gynecology and Obstetrics, University Medicine Göttingen, Robert-Koch-Str. 40, 37075, Göttingen, Germany.
Judith V BuseDepartment of Gynecology and Obstetrics, University Medicine Göttingen, Robert-Koch-Str. 40, 37075, Göttingen, Germany.
Christof LenzInstitute of Clinical Chemistry, University Medical Center Göttingen, Göttingen, Germany.
Gerd BauerschmitzDepartment of Gynecology and Obstetrics, University Medicine Göttingen, Robert-Koch-Str. 40, 37075, Göttingen, Germany.
Günter EmonsDepartment of Gynecology and Obstetrics, University Medicine Göttingen, Robert-Koch-Str. 40, 37075, Göttingen, Germany.
Carsten GründkerDepartment of Gynecology and Obstetrics, University Medicine Göttingen, Robert-Koch-Str. 40, 37075, Göttingen, Germany. grundker@med.uni-goettingen.de.
Universitätsmedizin Göttingen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

An altered consistency of tumor microenvironment facilitates the progression of the tumor towards metastasis. Here we combine data from secretome and proteome analysis using mass spectrometry with microarray data from mesenchymal transformed breast cancer cells (MCF-7-EMT) to elucidate the drivers of epithelial-mesenchymal transition (EMT) and cell invasion. Suppression of connective tissue growth factor (CTGF) reduced invasion in 2D and 3D invasion assays and expression of transforming growth factor-beta-induced protein ig-h3 (TGFBI), Zinc finger E-box-binding homeobox 1 (ZEB1) and lysyl oxidase (LOX), while the adhesion of cell-extracellular matrix (ECM) in mesenchymal transformed breast cancer cells is increased. In contrast, an enhanced expression of CTGF leads to an increased 3D invasion, expression of fibronectin 1 (FN1), secreted protein acidic and cysteine rich (SPARC) and CD44 and a reduced cell ECM adhesion. Gonadotropin-releasing hormone (GnRH) agonist Triptorelin reduces CTGF expression in a Ras homolog family member A (RhoA)-dependent manner. Our results suggest that CTGF drives breast cancer cell invasion in vitro and therefore could be an attractive therapeutic target for drug development to prevent the spread of breast cancer.

Indexed as

betaIG-H3 ProteinBreast NeoplasmsConnective Tissue Growth FactorEpithelial-Mesenchymal TransitionExtracellular MatrixExtracellular Matrix ProteinsFemaleFibronectinsGene ExpressionHumansHyaluronan ReceptorsMCF-7 CellsNeoplasm InvasivenessOsteonectinProtein-Lysine 6-OxidaserhoA GTP-Binding ProteinbetaIG-H3 ProteinCCN2 protein, humanCD44 protein, humanConnective Tissue Growth FactorExtracellular Matrix ProteinsFibronectinsFN1 protein, humanHyaluronan ReceptorsLOX protein, humanOsteonectinProtein-Lysine 6-OxidaserhoA GTP-Binding ProteinRHOA protein, humanSPARC protein, humanTransforming Growth Factor betaTriptorelin PamoateZEB1 protein, humanZinc Finger E-box-Binding Homeobox 1

Identifiers

PMID33087801
PMCPMC7578015
OpenAlexW3093568517

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.