Evidence map›Paper›PMID 23832051›Full record

ArticleIntegrative biology : quantitative biosciences from nano to macro2013

Transforming potential and matrix stiffness co-regulate confinement sensitivity of tumor cell migration.

Amit Pathak, Sanjay Kumar

Abstract read
In one paragraph

Article in Integrative biology : quantitative biosciences from nano to macro, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

39 citing papers in PubMed, 59 citations in OpenAlex.

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  13. Unjamming and collective migration in MCF10A breast cancer cell lines.Biochemical and biophysical research communications · 2020
    Article
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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

2 authors at 1 institution in 1 country.

Amit PathakDepartment of Bioengineering, University of California, Berkeley, CA 94720-1762, USA.
Sanjay Kumar
University of California, Berkeley · US

Funding

TRANS-NETWORK PROJECTSU54CA143836 · NCI · UNIVERSITY OF CALIFORNIA BERKELEY · PI LIPHARDT, JAN T. · 2009 to 2014
$15.1M
Cellular mechanobiology: Biophysics and therapeuticsDP2OD004213 · OD · UNIVERSITY OF CALIFORNIA BERKELEY · PI KUMAR, SANJAY · 2008 to 2008
$2.3M
NCI NIH HHS 1U54CA143836NCI NIH HHS U54 CA143836NIH HHS 1DP2OD004213NIH HHS DP2 OD004213
6 · The paper itself

Abstract

It is now well established that tumor cell invasion through tissue is strongly regulated by the microstructural and mechanical properties of the extracellular matrix (ECM). However, it remains unclear how these physical microenvironmental inputs are jointly processed with oncogenic lesions to drive invasion. In this study, we address this open question by combining a microfabricated polyacrylamide channel (μPAC) platform that enables independent control of ECM stiffness and confinement with an isogenically-matched breast tumor progression series in which the oncogenes ErbB2 and 14-3-3ζ are overexpressed independently or in tandem. We find that increasing channel confinement and overexpressing ErbB2 both promote cell migration to a similar degree when other parameters are kept constant. In contrast, 14-3-3ζ overexpression slows migration speed, and does so in a fashion that dwarfs effects of ECM confinement and stiffness. We also find that ECM stiffness dramatically enhances cell motility when combined with ErbB2 overexpression, demonstrating that biophysical cues and cell-intrinsic parameters promote cell invasion in an integrative manner. Morphometric analysis of cells inside the μPAC platform reveals that the rapid cell migration induced by narrow channels and ErbB2 overexpression are both accompanied by increased cell polarization. Disruption of this polarization occurs by pharmacological inhibition of Rac GTPase phenocopies 14-3-3ζ overexpression by reducing cell polarization and slowing migration. By systematically measuring migration speed as a function of matrix stiffness and confinement, we also quantify for the first time the sensitivity of migration speed to microchannel properties and transforming potential. These results demonstrate that oncogenic lesions and ECM biophysical properties can synergistically interact to drive invasive migration, and that both inputs may act through common molecular mechanisms to enhance migration speed.

Indexed as

14-3-3 ProteinsAcrylic ResinsCell Culture TechniquesCell Line, TumorCell MovementCell Transformation, NeoplasticErb-b2 Receptor Tyrosine KinasesExtracellular MatrixHumansHydrogel, Polyethylene Glycol DimethacrylateMicroscopy, ConfocalMicroscopy, Phase-ContrastNeoplasm InvasivenessNeoplasm MetastasisNeoplasmsPolyacrylamides14-3-3 ProteinsAcrylic ResinsErb-b2 Receptor Tyrosine KinasesHydrogel, Polyethylene Glycol DimethacrylatePolyacrylamidesrac GTP-Binding ProteinsSilicon

Identifiers

PMID23832051
PMCPMC3755126
OpenAlexW2108528666

What OpenQuestion holds

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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.