Evidence map›Paper›PMID 30515503›Full record

ArticleBiomaterials science2019

Macromolecular crowding tunes 3D collagen architecture and cell morphogenesis.

S K Ranamukhaarachchi, R N Modi, A Han, D O Velez, A Kumar, A J Engler, S I Fraley

Abstract read
In one paragraph

Article in Biomaterials science, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 10% 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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Matrix degradation enhances stress relaxation, regulating cell adhesion and spreading.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Degradability tunes ECM stress relaxation and cellular mechanics.bioRxiv : the preprint server for biology · 2024
    Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Highway toFrontiers in pharmacology · 2022
    Review
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 2 countries.

S K RanamukhaarachchiBioengineering, University of California San Diego Jacobs School of Engineering, La Jolla, California, USA. sifraley@ucsd.edu.
R N Modi
A Han
D O Velez
A Kumar
A J Engler
S I Fraley
University of California System · US

Funding

Biomaterial Mimicry of Dynamic Matrix Stiffening During Tumor ProgressionR01CA206880 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ENGLER, ADAM J, YANG, JING · 2016 to 2020
$1.8M
Predoctoral Training in Translational Musculoskeletal ResearchT32AR060712 · NIAMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI LIEBER, RICHARD L., SAH, ROBERT L · 2012 to 2016
$741k
NCI NIH HHS R01 CA206880NIAMS NIH HHS T32 AR060712
6 · The paper itself

Abstract

Collagen I is the primary extracellular matrix component of most solid tumors and influences metastatic progression. Collagen matrix engineering techniques are useful for understanding how this complex biomaterial regulates cancer cell behavior and for improving in vitro cancer models. Here, we establish an approach to tune collagen fibril architecture using PEG as an inert molecular crowding agent during gelation and cell embedding. We find that crowding produces matrices with tighter fibril networks that are less susceptible to proteinase mediated degradation, but does not significantly alter matrix stiffness. The resulting matrices have the effect of preventing cell spreading, confining cells, and reducing cell contractility. Matrix degradability and fibril length are identified as strong predictors of cell confinement. Further, the degree of confinement predicts whether breast cancer cells will ultimately undergo individual or collective behaviors. Highly confined breast cancer cells undergo morphogenesis to form either invasive networks reminiscent of aggressive tumors or gland and lobule structures reminiscent of normal breast epithelia. This morphological transition is accompanied by expression of cell-cell adhesion genes, including PECAM1 and ICAM1. Our study suggests that cell confinement, mediated by matrix architecture, is a design feature that tunes the transcriptional and morphogenic state of breast cancer cells.

Indexed as

Biocompatible MaterialsCell AdhesionCell Line, TumorCell ProliferationCell ShapeCollagen Type IHumansPolyethylene GlycolsBiocompatible MaterialsCollagen Type IPolyethylene Glycols

Identifiers

PMID30515503
PMCPMC6375559
OpenAlexW2903415252

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.