Evidence map›Paper›PMID 22232705›Full record

ArticleThe Journal of cell biology2012

A novel function for Cyclin A2: control of cell invasion via RhoA signaling.

Nikola Arsic, Nawal Bendris, Marion Peter, Christina Begon-Pescia, Cosette Rebouissou, Gilles Gadéa, Nathalie Bouquier, Frédéric Bibeau, Bénédicte Lemmers, Jean Marie Blanchard

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed
3.9field-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

87 citing papers in PubMed, 142 citations in OpenAlex.

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27 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 4 institutions in 1 country.

Nikola ArsicInstitut de Génétique Moléculaire de Montpellier, Centre National de la Recherche Scientifique, 34293 Montpellier, France.
Nawal Bendris
Marion Peter
Christina Begon-Pescia
Cosette Rebouissou
Gilles Gadéa
Nathalie Bouquier
Frédéric Bibeau
Bénédicte Lemmers
Jean Marie Blanchard
Institut de Génétique Moléculaire de Montpellier · FRCentre National de la Recherche Scientifique · FRUniversité de Montpellier · FRGefluc Languedoc Roussillon · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cyclin A2 plays a key role in cell cycle regulation. It is essential in embryonic cells and in the hematopoietic lineage yet dispensable in fibroblasts. In this paper, we demonstrate that Cyclin A2-depleted cells display a cortical distribution of actin filaments and increased migration. These defects are rescued by restoration of wild-type Cyclin A2, which directly interacts with RhoA, or by a Cyclin A2 mutant unable to associate with Cdk. In vitro, Cyclin A2 potentiates the exchange activity of a RhoA-specific guanine nucleotide exchange factor. Consistent with this, Cyclin A2 depletion enhances migration of fibroblasts and invasiveness of transformed cells via down-regulation of RhoA activity. Moreover, Cyclin A2 expression is lower in metastases relative to primary colon adenocarcinoma in matched human tumors. All together, these data show that Cyclin A2 negatively controls cell motility by promoting RhoA activation, thus demonstrating a novel Cyclin A2 function in cytoskeletal rearrangements and cell migration.

Indexed as

Neoplasm InvasivenessActin CytoskeletonAdenocarcinomaAnimalsCell Line, TumorCell MovementColorectal NeoplasmsCyclin A2Down-RegulationFocal AdhesionsHumansMiceNIH 3T3 CellsrhoA GTP-Binding ProteinRNA InterferenceSignal TransductionCyclin A2rhoA GTP-Binding Protein

Identifiers

PMID22232705
PMCPMC3255987
OpenAlexW1995947885

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.