Evidence map›Paper›PMID 27027351›Full record

ArticleOncotarget2016

Adipose microenvironment promotes triple negative breast cancer cell invasiveness and dissemination by producing CCL5.

Vittoria D'Esposito, Domenico Liguoro, Maria Rosaria Ambrosio, Francesca Collina, Monica Cantile, Rosa Spinelli, Gregory Alexander Raciti, Claudia Miele, Rossella Valentino, Pietro Campiglia and 6 more

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 99 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
99citing papers in PubMed, 2 pooled it
6.9field-weighted citation impact, top 2% 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

99 citing papers in PubMed, 2 syntheses or guidelines pooled it, 137 citations in OpenAlex.

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39 more citing papers are in PubMed but not listed here.

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

16 authors at 3 institutions in 1 country.

Vittoria D'EspositoDepartment of Translational Medicine, Federico II University of Naples and URT "Genomic of Diabetes" of Institute of Experimental Endocrinology and Oncology, National Council of Research (CNR), Naples, Italy.
Domenico LiguoroDepartment of Translational Medicine, Federico II University of Naples and URT "Genomic of Diabetes" of Institute of Experimental Endocrinology and Oncology, National Council of Research (CNR), Naples, Italy.
Maria Rosaria AmbrosioDepartment of Translational Medicine, Federico II University of Naples and URT "Genomic of Diabetes" of Institute of Experimental Endocrinology and Oncology, National Council of Research (CNR), Naples, Italy.
Francesca CollinaPathology Unit, National Institute of Tumors, Fondazione "G. Pascale", Naples, Italy.
Monica CantilePathology Unit, National Institute of Tumors, Fondazione "G. Pascale", Naples, Italy.
Rosa SpinelliDepartment of Translational Medicine, Federico II University of Naples and URT "Genomic of Diabetes" of Institute of Experimental Endocrinology and Oncology, National Council of Research (CNR), Naples, Italy.
Gregory Alexander RacitiDepartment of Translational Medicine, Federico II University of Naples and URT "Genomic of Diabetes" of Institute of Experimental Endocrinology and Oncology, National Council of Research (CNR), Naples, Italy.
Claudia MieleDepartment of Translational Medicine, Federico II University of Naples and URT "Genomic of Diabetes" of Institute of Experimental Endocrinology and Oncology, National Council of Research (CNR), Naples, Italy.
Rossella ValentinoDepartment of Translational Medicine, Federico II University of Naples and URT "Genomic of Diabetes" of Institute of Experimental Endocrinology and Oncology, National Council of Research (CNR), Naples, Italy.
Pietro CampigliaDepartment of Pharmacy, University of Salerno, Salerno, Italy.
Michelino De LaurentiisDepartment of Breast Surgery and Cancer Prevention; National Institute of Tumors, Fondazione "G. Pascale", Naples, Italy.
Maurizio Di BonitoPathology Unit, National Institute of Tumors, Fondazione "G. Pascale", Naples, Italy.
Gerardo BottiPathology Unit, National Institute of Tumors, Fondazione "G. Pascale", Naples, Italy.
Renato FrancoPathology Unit, National Institute of Tumors, Fondazione "G. Pascale", Naples, Italy.
Francesco BeguinotDepartment of Translational Medicine, Federico II University of Naples and URT "Genomic of Diabetes" of Institute of Experimental Endocrinology and Oncology, National Council of Research (CNR), Naples, Italy.
Pietro FormisanoDepartment of Translational Medicine, Federico II University of Naples and URT "Genomic of Diabetes" of Institute of Experimental Endocrinology and Oncology, National Council of Research (CNR), Naples, Italy.
Institute for Experimental Endocrinology and Oncology · ITIstituto Nazionale Tumori IRCCS "Fondazione G. Pascale" · ITUniversity of Salerno · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Growing evidence indicates that adiposity is associated with raised cancer incidence, morbidity and mortality. In a subset of tumors, cancer cell growth and/or metastasis predominantly occur in adipocyte-rich microenvironment. Indeed, adipocytes represent the most abundant cell types surrounding breast cancer cells. We have studied the mechanisms by which peritumoral human adipose tissue contributes to Triple Negative Breast Cancer (TNBC) cell invasiveness and dissemination.Co-culture with human adipocytes enhanced MDA-MB231 cancer cell invasiveness. Adipocytes cultured in high glucose were 2-fold more active in promoting cell invasion and motility compared to those cultured in low glucose. This effect is induced, at least in part, by the CC-chemokine ligand 5 (CCL5). Indeed, CCL5 inhibition by specific peptides and antibodies reduced adipocyte-induced breast cancer cell migration and invasion. CCL5 immuno-detection in peritumoral adipose tissue of women with TNBC correlated with lymph node (p-value = 0.04) and distant metastases (p-value = 0.001). A positive trend was also observed between CCL5 expression and glycaemia. Finally, Kaplan-Meier curves showed a negative correlation between CCL5 staining in the peritumoral adipose tissue and overall survival of patients (p-value = 0.039).Thus, inhibition of CCL5 in adipose microenvironment may represent a novel approach for the therapy of highly malignant TNBC.

Indexed as

Cell MovementAdipocytesAdipose TissueAdultCell Line, TumorCellular MicroenvironmentChemokine CCL5Coculture TechniquesFemaleGene Expression Regulation, NeoplasticHumansKaplan-Meier EstimateLymphatic MetastasisMCF-7 CellsMiddle AgedNeoplasm InvasivenessChemokine CCL5adipose tissuecytokinesdiabetesobesitytriple negative breast cancer

Identifiers

PMID27027351
PMCPMC5029717
OpenAlexW2323501321

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.