Evidence map›Paper›PMID 29588395›Full record

ArticleJournal of cell science2018

Substratum stiffness tunes proliferation downstream of Wnt3a in part by regulating integrin-linked kinase and frizzled-1.

Siyang Han, Mei-Fong Pang, Celeste M Nelson

Open access · bronzeAbstract read
In one paragraph

Article in Journal of cell science, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

20 citing papers in PubMed, 41 citations in OpenAlex.

  1. Review
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  4. Cell signaling characterization for spatial transcriptomics (ST) data using network analysis.Complex networks & their applications. International Conference on Complex Networks and Their Applications · 2025
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  16. A spatial model of YAP/TAZ signaling reveals how stiffness, dimensionality, and shape contribute to emergent outcomes.Proceedings of the National Academy of Sciences of the United States of America · 2021
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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

3 authors at 1 institution in 1 country.

Siyang HanDepartment of Molecular Biology, Princeton University, Princeton, NJ 08544, USA.
Mei-Fong PangDepartment of Chemical & Biological Engineering, Princeton University, Princeton, NJ 08544, USA.
Celeste M NelsonDepartment of Molecular Biology, Princeton University, Princeton, NJ 08544, USA celesten@princeton.edu.ORCID 0000-0001-9973-8870
Princeton University · US

Funding

Engineered Invasive Human Breast Tumors with Integrated Capillaries and LymphaticsU01CA214292 · NCI · BOSTON UNIVERSITY (CHARLES RIVER CAMPUS) · PI NELSON, CELESTE M, TIEN, JOE Y · 2017 to 2021
$3.2M
Biophysical and Biochemical Effects of the ECM on Breast Epithelial CellsR01CA187692 · NCI · PRINCETON UNIVERSITY · PI NELSON, CELESTE M, RADISKY, DEREK C · 2015 to 2019
$2.1M
Mechanical Regulation of Mesenchyme and Mammalian Lung DevelopmentR01HL120142 · NHLBI · PRINCETON UNIVERSITY · PI NELSON, CELESTE M · 2014 to 2017
$1.6M
Mechanical regulation of branching morphogenesisR21HL110335 · NHLBI · PRINCETON UNIVERSITY · PI NELSON, CELESTE M · 2011 to 2012
$443k
Exogenous Fluid Forces and Branching of the Mammalian LungR21HL118532 · NHLBI · PRINCETON UNIVERSITY · PI NELSON, CELESTE M · 2014 to 2015
$442k
Howard Hughes Medical InstituteNCI NIH HHS R01 CA187692NCI NIH HHS U01 CA214292NHLBI NIH HHS R01 HL120142NHLBI NIH HHS R21 HL110335NHLBI NIH HHS R21 HL118532
6 · The paper itself

Abstract

The Wnt/β-catenin pathway controls a variety of cellular behaviors, aberrant activation of which are associated with tumor progression in several types of cancer. The same cellular behaviors are also affected by the mechanical properties of the extracellular matrix (ECM) substratum, which induces signaling through integrins and integrin-linked kinase (ILK). Here, we examined the role of substratum stiffness in the regulation of cell proliferation downstream of Wnt3a. We found that treatment with Wnt3a increased proliferation of cells cultured on stiff substrata, with compliances characteristic of breast tumors, but not of cells on soft substrata, with compliances comparable to that of normal mammary tissue. Depleting ILK rendered cells unresponsive to Wnt3a on both substrata. Ectopic expression of ILK permitted Wnt3a to induce proliferation of cells on both microenvironments, although proliferation on soft substrata remained lower than that on stiff substrata. We further showed that ILK regulates expression of the Wnt receptor frizzled-1 (

Indexed as

Cell ProliferationCells, CulturedExtracellular MatrixFrizzled ReceptorsHumansProtein Serine-Threonine KinasesScaffold Protein ILKWnt3A ProteinFrizzled ReceptorsProtein Serine-Threonine KinasesScaffold Protein ILKWnt3A ProteinComplianceMechanosensingMechanotransductionMorphodynamicsMorphogenesis

Identifiers

PMID29588395
PMCPMC5963841
OpenAlexW2794446484

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.