Evidence map›Paper›PMID 28877984›Full record

ArticleMolecular biology of the cell2017

α5β1-Integrin promotes tension-dependent mammary epithelial cell invasion by engaging the fibronectin synergy site.

Y A Miroshnikova, G I Rozenberg, L Cassereau, M Pickup, J K Mouw, G Ou, K L Templeman, E-I Hannachi, K J Gooch, A L Sarang-Sieminski and 2 more

Abstract read
In one paragraph

Article in Molecular biology of the cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
4.6field-weighted citation impact, top 4% 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

45 citing papers in PubMed, 74 citations in OpenAlex.

  1. Review
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  4. Integrin-Piezo1 Axis Drives ECM Remodeling and Invasion of 3D Breast Epithelium.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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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

12 authors at 3 institutions in 1 country.

Y A MiroshnikovaDepartment of Surgery, Center for Bioengineering and Tissue Regeneration, University of California, San Francisco, San Francisco, CA 94143.
G I RozenbergInstitute for Medicine and Engineering, University of Pennsylvania, Philadelphia, PA 19104.
L CassereauDepartment of Surgery, Center for Bioengineering and Tissue Regeneration, University of California, San Francisco, San Francisco, CA 94143.
M PickupDepartment of Surgery, Center for Bioengineering and Tissue Regeneration, University of California, San Francisco, San Francisco, CA 94143.
J K MouwDepartment of Surgery, Center for Bioengineering and Tissue Regeneration, University of California, San Francisco, San Francisco, CA 94143.
G OuDepartment of Surgery, Center for Bioengineering and Tissue Regeneration, University of California, San Francisco, San Francisco, CA 94143.
K L TemplemanWoodruff School of Mechanical Engineering, Petit Institute for Bioengineering and Bioscience, Georgia Institute of Technology, Atlanta, GA 30332.
E-I HannachiWoodruff School of Mechanical Engineering, Petit Institute for Bioengineering and Bioscience, Georgia Institute of Technology, Atlanta, GA 30332.
K J GoochInstitute for Medicine and Engineering, University of Pennsylvania, Philadelphia, PA 19104.
A L Sarang-SieminskiInstitute for Medicine and Engineering, University of Pennsylvania, Philadelphia, PA 19104.
A J GarcíaWoodruff School of Mechanical Engineering, Petit Institute for Bioengineering and Bioscience, Georgia Institute of Technology, Atlanta, GA 30332.
V M WeaverDepartment of Surgery, Center for Bioengineering and Tissue Regeneration, University of California, San Francisco, San Francisco, CA 94143 valerie.weaver@ucsf.edu.
University of California, San Francisco · USGeorgia Institute of Technology · USUniversity of Pennsylvania · US

Funding

Project 3: Physical and Metabolic Constraints of Cancer Cell InvasionU54CA210184 · NCI · CORNELL UNIVERSITY · PI ZIPFEL, WARREN R · 2016 to 2020
$10.2M
TUMOR BIOLOGYT32CA009151 · NCI · STANFORD UNIVERSITY · PI CLEARY, MICHAEL L · 1985 to 2014
$5.5M
ECM geometrical and mechanical properties modulate RTK signalingU01CA202241 · NCI · UNIVERSITY OF CALIFORNIA BERKELEY · PI GROVES, JAY T., WEAVER, VALERIE MARIE · 2015 to 2019
$3.3M
A biophysical stromal basis for radiation sensitivity in ductal carcinoma in situR01CA174929 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI PARK, CATHERINE C, WEAVER, VALERIE MARIE · 2014 to 2018
$3.1M
Tension-Stat3-miR-mediated metastasisR01CA192914 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI SEEWALDT, VICTORIA L., WEAVER, VALERIE MARIE · 2015 to 2019
$2.9M
Focal Adhesions in Cell Adhesion StrengtheningR01GM065918 · NIGMS · GEORGIA INSTITUTE OF TECHNOLOGY · PI GARCIA, ANDRES J · 2002 to 2011
$2.6M
Glycocalyx and NCOR2-Notch-Mediated Stemness in Glioblastoma AggressivenessF31CA180422 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MIROSHNIKOVA, YEKATERINA ANDREEVNA · 2014 to 2015
$48k
NCI NIH HHS F31 CA180422NCI NIH HHS R01 CA192914NCI NIH HHS T32 CA009151NCI NIH HHS U01 CA202241NCI NIH HHS U54 CA210184NIGMS NIH HHS R01 GM065918
6 · The paper itself

Abstract

Tumors are fibrotic and characterized by abundant, remodeled, and cross-linked collagen that stiffens the extracellular matrix stroma. The stiffened collagenous stroma fosters malignant transformation of the tissue by increasing tumor cell tension to promote focal adhesion formation and potentiate growth factor receptor signaling through kinase. Importantly, collagen cross-linking requires fibronectin (FN). Fibrotic tumors contain abundant FN, and tumor cells frequently up-regulate the FN receptor α5β1 integrin. Using transgenic and xenograft models and tunable two- and three-dimensional substrates, we show that FN-bound α5β1 integrin promotes tension-dependent malignant transformation through engagement of the synergy site that enhances integrin adhesion force. We determined that ligation of the synergy site of FN permits tumor cells to engage a zyxin-stabilized, vinculin-linked scaffold that facilitates nucleation of phosphatidylinositol (3,4,5)-triphosphate at the plasma membrane to enhance phosphoinositide 3-kinase (PI3K)-dependent tumor cell invasion. The data explain why rigid collagen fibrils potentiate PI3K activation to promote malignancy and offer a perspective regarding the consistent up-regulation of α5β1 integrin and FN in many tumors and their correlation with cancer aggression.

Indexed as

AnimalsBreastCell AdhesionCell MembraneCells, CulturedCytokinesEpithelial CellsExtracellular MatrixFemaleFibronectinsHeterograftsHumansIntegrin alpha5beta1IntegrinsMiceMice, TransgenicCytokinesFibronectinsFN1 protein, humanIntegrin alpha5beta1IntegrinsPhosphatidylinositol 3-Kinases

Identifiers

PMID28877984
PMCPMC5662256
OpenAlexW2751895094

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.