Evidence map›Paper›PMID 29450424›Full record

ArticleIntegrative biology : quantitative biosciences from nano to macro2018

CD44v6 increases gastric cancer malignant phenotype by modulating adipose stromal cell-mediated ECM remodeling.

Bianca N Lourenço, Nora L Springer, Daniel Ferreira, Carla Oliveira, Pedro L Granja, Claudia Fischbach

Abstract read
In one paragraph

Article in Integrative biology : quantitative biosciences from nano to macro, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.5field-weighted citation impact, top 20% 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

11 citing papers in PubMed, 23 citations in OpenAlex.

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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

6 authors at 2 institutions in 2 countries.

Bianca N LourençoNancy E. and Peter C. Meinig School of Biomedical Engineering, Cornell University, 157 Weill Hall, Ithaca, NY 14853, USA. cf99@cornell.edu and i3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto, Portugal and INEB - Instituto de Engenharia Biomédica, Universidade do Porto, Portugal and IPATIMUP - Institute of Molecular Pathology and Immunology of the University of Porto, Portugal and Faculdade de Engenharia, Universidade do Porto, Portugal.ORCID 0000-0001-6421-0021
Nora L SpringerNancy E. and Peter C. Meinig School of Biomedical Engineering, Cornell University, 157 Weill Hall, Ithaca, NY 14853, USA. cf99@cornell.edu and Biological and Biomedical Sciences, Cornell University, Ithaca, NY, USA.ORCID 0000-0003-4543-7313
Daniel Ferreirai3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto, Portugal and INEB - Instituto de Engenharia Biomédica, Universidade do Porto, Portugal and IPATIMUP - Institute of Molecular Pathology and Immunology of the University of Porto, Portugal and Instituto de Ciências Biomédicas Abel Salazar, Universidade do Porto, Portugal.ORCID 0000-0002-9712-1460
Carla Oliveirai3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto, Portugal and IPATIMUP - Institute of Molecular Pathology and Immunology of the University of Porto, Portugal and Departamento de Patologia e Oncologia, Faculdade de Medicina, Universidade do Porto, Portugal.ORCID 0000-0001-8340-2264
Pedro L Granjai3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto, Portugal and INEB - Instituto de Engenharia Biomédica, Universidade do Porto, Portugal and Faculdade de Engenharia, Universidade do Porto, Portugal and Instituto de Ciências Biomédicas Abel Salazar, Universidade do Porto, Portugal.ORCID 0000-0003-2761-4929
Claudia FischbachNancy E. and Peter C. Meinig School of Biomedical Engineering, Cornell University, 157 Weill Hall, Ithaca, NY 14853, USA. cf99@cornell.edu and Kavli Institute at Cornell for Nanoscale Science, Cornell University, Ithaca, NY, USA.ORCID 0000-0002-9368-0150
Universidade do Porto · PTCornell University · US

Funding

Project 3: Physical and Metabolic Constraints of Cancer Cell InvasionU54CA210184 · NCI · CORNELL UNIVERSITY · PI CANTLEY, LEWIS C., FISCHBACH, CLAUDIA · 2016 to 2020
$10.2M
(PQA2) Interstitial stiffness as a physicochemical modulator of obesity-induced bR01CA185293 · NCI · CORNELL UNIVERSITY · PI FISCHBACH, CLAUDIA · 2014 to 2017
$1.3M
Zeiss LSM710 Confocal Microscope for Shared Imaging FacilityS10RR025502 · NCRR · CORNELL UNIVERSITY · PI WILLIAMS, REBECCA M · 2009 to 2009
$500k
NCI NIH HHS R01 CA185293NCI NIH HHS U54 CA210184NCRR NIH HHS S10 RR025502
6 · The paper itself

Abstract

CD44, an abundantly expressed adhesion molecule, and its alternative splice variants have been associated with tumorigenesis and metastasis. In the context of gastric cancer (GC), de novo expression of CD44 variant 6 (CD44v6) is found in more than 60% of GCs, but its role in the pathogenesis and progression of this type of cancer remains unclear. Using a combination of media conditioning experiments and decellularized extracellular matrices (ECMs), this study investigates the hypothesis that CD44v6 overexpression enhances tumor cell malignant behavior by modulating stromal cell-mediated ECM remodeling. Our findings indicate that soluble factors secreted by CD44v6 expressing GC cells particularly increase proliferation and myofibroblastic differentiation of adipose stromal cells (ASCs). These changes in ASC phenotype mediate the deposition of fibrotic/desmoplastic ECM that, in turn, stimulates GC proliferation and inhibits GC clustering. Pharmacological inhibition of matrix metalloproteinase (MMP) activity in tumor cells abrogated matrix-induced changes in tumor cell malignant behavior. Additionally, studies in mice confirmed the pathological relevance of CD44v6 expression and consequential changes in ECM remodeling to gastric tumorigenesis in vivo. Collectively, these results indicate a direct link between CD44v6, ECM remodeling, and GC malignant behavior opening new insights into potential CD44v6-targeted therapies.

Indexed as

3T3 CellsAdipose TissueAnimalsCell AdhesionCell Line, TumorCell ProliferationCell Transformation, NeoplasticCulture Media, ConditionedDisease ProgressionExtracellular MatrixFemaleFibrosisHumansHyaluronan ReceptorsMiceMice, Inbred NODCD44v6 antigenCulture Media, ConditionedHyaluronan Receptors

Identifiers

PMID29450424
PMCPMC5988203
OpenAlexW2787018508

What OpenQuestion holds

Textmetadata
LicenceTDM
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.