Evidence map›Paper›PMID 31251330›Full record

ArticleIntegrative biology : quantitative biosciences from nano to macro2019

3D collagen architecture regulates cell adhesion through degradability, thereby controlling metabolic and oxidative stress.

Daniel O Velez, Sural K Ranamukhaarachchi, Aditya Kumar, Rishi N Modi, Esther W Lim, Adam J Engler, Christian M Metallo, Stephanie I Fraley

Abstract read
In one paragraph

Article in Integrative biology : quantitative biosciences from nano to macro, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

23 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. 3DACS biomaterials science & engineering · 2023
    Pooled it
  2. Monocytes use protrusive forces to generate migration paths in viscoelastic collagen-based extracellular matrices.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  3. Matrix degradation enhances stress relaxation, regulating cell adhesion and spreading.Proceedings of the National Academy of Sciences of the United States of America · 2025
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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

8 authors.

Daniel O VelezBioengineering Department, University of California San Diego, CA, USA.
Sural K RanamukhaarachchiBioengineering Department, University of California San Diego, CA, USA.
Aditya KumarBioengineering Department, University of California San Diego, CA, USA.
Rishi N ModiBioengineering Department, University of California San Diego, CA, USA.
Esther W LimBioengineering Department, University of California San Diego, CA, USA.
Adam J EnglerBioengineering Department, University of California San Diego, CA, USA.
Christian M MetalloBioengineering Department, University of California San Diego, CA, USA.
Stephanie I FraleyBioengineering Department, University of California San Diego, CA, USA.

Funding

Training in Multi-Scale Analysis of Biological Structure and FunctionT32EB009380 · NIBIB · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Andrew D. McCulloch, Padmini Rangamani · 2009 to 2026
$4.8M
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
Exploiting Metabloic Defects in Tumors with Mutant IDH1 and IDH2R01CA188652 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI METALLO, CHRISTIAN MICHAEL · 2014 to 2018
$1.6M
Modeling and analysis of the mechanochemical processes that govern clathrin-mediated endocytosisR01GM132106 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI RANGAMANI, PADMINI · 2020 to 2024
$1.5M
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 CA188652NCI NIH HHS R01 CA206880NIAMS NIH HHS T32 AR060712NIBIB NIH HHS T32 EB009380NIGMS NIH HHS R01 GM132106
6 · The paper itself

Abstract

The collagen-rich tumor microenvironment plays a critical role in directing the migration behavior of cancer cells. 3D collagen architectures with small pores have been shown to confine cells and induce aggressive collective migration, irrespective of matrix stiffness and density. However, it remains unclear how cells sense collagen architecture and transduce this information to initiate collective migration. Here, we tune collagen architecture and analyze its effect on four core cell-ECM interactions: cytoskeletal polymerization, adhesion, contractility, and matrix degradation. From this comprehensive analysis, we deduce that matrix architecture initially modulates cancer cell adhesion strength, and that this results from architecture-induced changes to matrix degradability. That is, architectures with smaller pores are less degradable, and degradability is required for cancer cell adhesion to 3D fibrilar collagen. The biochemical consequences of this 3D low-attachment state are similar to those induced by suspension culture, including metabolic and oxidative stress. One distinction from suspension culture is the induction of collagen catabolism that occurs in 3D low-attachment conditions. Cells also upregulate Snail1 and Notch signaling in response to 3D low-attachment, which suggests a mechanism for the emergence of collective behaviors.

Indexed as

Cell AdhesionOxidative StressCell Line, TumorCell MovementCollagenCytoskeletonExtracellular MatrixGene Expression ProfilingHumansMicroscopy, Atomic ForceMicroscopy, ConfocalNeoplasmsReceptor, Notch1RheologyShear StrengthSignal TransductionCollagenNOTCH1 protein, humanReceptor, Notch1SNAI1 protein, humanSnail Family Transcription Factors

Identifiers

PMID31251330
PMCPMC6657753

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.