Evidence map›Paper›PMID 16624865›Full record

ArticleMolecular biology of the cell2006

Phosphoinositide-3 kinase-Rac1-c-Jun NH2-terminal kinase signaling mediates collagen I-induced cell scattering and up-regulation of N-cadherin expression in mouse mammary epithelial cells.

Yasushi Shintani, Margaret J Wheelock, Keith R Johnson

Open access · greenAbstract read
In one paragraph

Article in Molecular biology of the cell, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

46 citing papers in PubMed, 85 citations in OpenAlex.

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  17. Epithelial cell polarity determinant CRB3 in cancer development.International journal of biological sciences · 2015
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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 2 institutions in 1 country.

Yasushi ShintaniDepartment of Oral Biology, Eppley Institute for Research in Cancer and Allied Diseases, and Eppley Cancer Center, University of Nebraska Medical Center, Omaha, NE 68198-7696, USA.
Margaret J Wheelock
Keith R Johnson
Nebraska Medical Center · USUniversity of Nebraska Medical Center · US

Funding

UNMC/EPPLEY CANCER CENTER SUPPORT GRANTP30CA036727 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI Apar Kishor Ganti · 1985 to 2026
$55.0M
ASPECTS OF CADHERIN/CATENIN COMPLEXESR01GM051188 · NIGMS · UNIVERSITY OF TOLEDO · PI JOHNSON, KEITH R · 1994 to 2009
$3.4M
CADHERINS IN ORAL SQUAMOUS CELL CARCINOMASR01DE012308 · NIDCR · UNIVERSITY OF TOLEDO · PI JOHNSON, KEITH R · 1998 to 2007
$2.6M
NCI NIH HHS P30 CA036727NCI NIH HHS P30 CA36727NIDCR NIH HHS R01 DE012308NIDCR NIH HHS R01-DE12308NIGMS NIH HHS R01 GM051188NIGMS NIH HHS R01-GM51188
6 · The paper itself

Abstract

During epithelial-to-mesenchymal transitions (EMTs), cells must change their interactions with one another and with their extracellular matrix in a synchronized manner. To characterize signaling pathways cells use to coordinate these changes, we used NMuMG mammary epithelial cells. We showed that these cells become fibroblastic and scattered, with increased N-cadherin expression when cultured on collagen I. Rac1 and c-Jun NH2-terminal kinase (JNK) were activated when cells were plated on collagen I, and dominant inhibitory Rac1 (RacN17) or inhibition of JNK signaling prevented collagen I-induced morphological changes and N-cadherin up-regulation. Furthermore, inhibiting phosphoinositide-3 kinase (PI3K) activity prevented Rac1 and JNK activation as well as collagen I-induced N-cadherin up-regulation. These data implicate PI3K-Rac1-JNK signaling in collagen I-induced changes in NMuMG cells. To establish a role for N-cadherin in collagen I-induced cell scattering, we generated N-cadherin overexpressing and knockdown NMuMG cells and showed that knocking down N-cadherin expression prevented collagen I-induced morphological changes. Motility assays showed that cells overexpressing N-cadherin were significantly more motile than mock-transfected cells and that N-cadherin-mediated motility was collagen I dependent. In addition, we showed that cord formation and branching in three-dimensional culture (EMT-dependent events) required N-cadherin expression and PI3K-Rac1-JNK signaling.

Indexed as

Cell MovementAnimalsCadherinsCell Culture TechniquesCell DifferentiationCells, CulturedCollagen Type IEpithelial CellsIntegrinsJNK Mitogen-Activated Protein KinasesMammary Glands, AnimalMesodermMicePhosphatidylinositol 3-Kinasesrac1 GTP-Binding ProteinSignal TransductionCadherinsCollagen Type IIntegrinsJNK Mitogen-Activated Protein KinasesPhosphatidylinositol 3-Kinasesrac1 GTP-Binding Protein

Identifiers

PMID16624865
PMCPMC1483033
OpenAlexW2111183194

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.