Evidence map›Paper›PMID 20871938›Full record

ArticleIntegrative biology : quantitative biosciences from nano to macro2010

Microfluidic platform for chemotaxis in gradients formed by CXCL12 source-sink cells.

Yu-Suke Torisawa, Bobak Mosadegh, Tommaso Bersano-Begey, Jessica M Steele, Kathryn E Luker, Gary D Luker, Shuichi Takayama

Abstract read
In one paragraph

Article in Integrative biology : quantitative biosciences from nano to macro, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
4.7field-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

38 citing papers in PubMed, 78 citations in OpenAlex.

  1. Article
  2. Article
  3. Patterning Neuroepithelial Cell SheetACS biomaterials science & engineering · 2021
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  13. Progress towards understanding heterotypic interactions in multi-culture models of breast cancer.Integrative biology : quantitative biosciences from nano to macro · 2016
    Review
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  16. 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

7 authors at 2 institutions in 1 country.

Yu-Suke TorisawaDepartment of Biomedical Engineering, University of Michigan, Ann Arbor, MI 48109, USA.
Bobak Mosadegh
Tommaso Bersano-Begey
Jessica M Steele
Kathryn E Luker
Gary D Luker
Shuichi Takayama
University of Michigan–Ann Arbor · USIn-Q-Tel · US

Funding

Small Animal Imaging CoreP50CA093990 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ROSS, BRIAN D. · 2002 to 2012
$19.0M
Microfluidic Models of Metastatic CancerR01CA136829 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LUKER, GARY D · 2009 to 2013
$1.5M
Molecular Imaging of Chemokine Receptor SignalingR01CA136553 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LUKER, GARY D · 2009 to 2013
$1.5M
NCI NIH HHS P50 CA093990NCI NIH HHS P50CA093990NCI NIH HHS R01 CA136553NCI NIH HHS R01CA136553NCI NIH HHS R01 CA136829NCI NIH HHS R01CA136829
6 · The paper itself

Abstract

Chemokine CXCL12 promotes CXCR4-dependent chemotaxis of cancer cells to characteristic organs and tissues, leading to metastatic disease. This study was designed to investigate how cells expressing CXCR7 regulate chemotaxis of a separate population of CXCR4 cells under physiologic conditions in which cells are exposed to gradients of CXCL12. We recapitulated a cancer-stroma microenvironment by patterning CXCR4-expressing cancer cells in microchannels at spatially defined positions relative to CXCL12-producing cells and CXCR7-expressing cells. CXCR7 scavenges and degrades CXCL12, which has been proposed to facilitate CXCR4-dependent chemotaxis through a source-sink model. Using the microchannel device, we demonstrated that chemotaxis of CXCR4 cells depended critically on the presence and location of CXCR7 cells (sink) relative to chemokine secreting cells (source). Furthermore, inhibiting CXCR4 on migrating cells or CXCR7 on sink cells blocked CXCR4-dependent chemotaxis toward CXCL12, showing that the device can identify new therapeutic agents that block migration by targeting chemoattractant scavenging receptors. Our system enables efficient chemotaxis under much shallower yet more physiological chemoattractant gradients by generating an in vitro microenvironment where combinations of cellular products may be secreted along with formation of a chemoattractant gradient. In addition to elucidating mechanisms of CXCL-12 mediated chemotaxis, this simple and robust method can be broadly useful for engineering multiple microenvironments to investigate intercellular communication.

Indexed as

Breast NeoplasmsCell Line, TumorChemokine CXCL12ChemotaxisFemaleHEK293 CellsHumansMicrofluidic Analytical TechniquesModels, BiologicalReceptors, CXCRReceptors, CXCR4Signal TransductionACKR3 protein, humanChemokine CXCL12CXCL12 protein, humanCXCR4 protein, humanReceptors, CXCRReceptors, CXCR4

Identifiers

PMID20871938
PMCPMC4128891
OpenAlexW2052755392

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.