Evidence map›Paper›PMID 28591581›Full record

ArticleCell reports2017

Laminin-111 and the Level of Nuclear Actin Regulate Epithelial Quiescence via Exportin-6.

Ana Paula Zen Petisco Fiore, Virginia A Spencer, Hidetoshi Mori, Hernandes F Carvalho, Mina J Bissell, Alexandre Bruni-Cardoso

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2017. 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
3.8field-weighted citation impact, top 6% 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, 81 citations in OpenAlex.

  1. Article
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  4. Nuclear actin is a critical regulator ofbioRxiv : the preprint server for biology · 2024
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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

6 authors at 5 institutions in 2 countries.

Ana Paula Zen Petisco FioreDepartamento de Bioquímica, Instituto de Química, Universidade de São Paulo, São Paulo, SP 05508-000, Brazil.
Virginia A SpencerThermo Fisher Scientific, Frederick, MD 21703, USA.
Hidetoshi MoriLife Science Division, Lawrence Berkeley National Laboratory, Berkeley, CA 94720, USA; Center for Comparative Medicine, University of California, Davis, Davis, CA 95616, USA.
Hernandes F CarvalhoINFABiC - National Institute of Science and Technology on Photonics Applied to Cell Biology, Campinas, SP 13083-862, Brazil; Structural and Functional Biology Department, Institute of Biology, State University of Campinas, Campinas, SP 13083-865, Brazil.
Mina J BissellLife Science Division, Lawrence Berkeley National Laboratory, Berkeley, CA 94720, USA. Electronic address: mjbissell@lbl.gov.
Alexandre Bruni-CardosoDepartamento de Bioquímica, Instituto de Química, Universidade de São Paulo, São Paulo, SP 05508-000, Brazil; Life Science Division, Lawrence Berkeley National Laboratory, Berkeley, CA 94720, USA; INFABiC - National Institute of Science and Technology on Photonics Applied to Cell Biology, Campinas, SP 13083-862, Brazil. Electronic address: brunicar@iq.usp.br.
Brazilian Biosciences National Laboratory · BRLawrence Berkeley National Laboratory · USThermo Fisher Scientific (United States) · USUniversidade de São Paulo · BRUniversity of California, Davis · US

Funding

TRANS-NETWORK PROJECTSU54CA143836 · NCI · UNIVERSITY OF CALIFORNIA BERKELEY · PI LIPHARDT, JAN T. · 2009 to 2014
$15.1M
Definition of the Microenvironment in Breast CancerR01CA064786 · NCI · UNIVERSITY OF CALIF-LAWRENC BERKELEY LAB · PI BISSELL, MINA · 1995 to 2020
$6.1M
Definition of Microenvironment in Breast CancerR37CA064786 · NCI · UNIVERSITY OF CALIF-LAWRENC BERKELEY LAB · PI BISSELL, MINA · 2009 to 2013
$2.0M
NCI NIH HHS R01 CA064786NCI NIH HHS R37 CA064786NCI NIH HHS U54 CA143836
6 · The paper itself

Abstract

Nuclear actin (N-actin) is known to participate in the regulation of gene expression. We showed previously that N-actin levels mediate the growth and quiescence of mouse epithelial cells in response to laminin-111 (LN1), a component of the mammary basement membrane (BM). We know that BM is defective in malignant cells, and we show here that it is the LN1/N-actin pathway that is aberrant in human breast cancer cells, leading to continuous growth. Photobleaching assays revealed that N-actin exit in nonmalignant cells begins as early as 30 min after LN1 treatment. LN1 attenuates the PI3K pathway leading to upregulation of exportin-6 (XPO6) activity and shuttles actin out of the nucleus. Silencing XPO6 prevents quiescence. Malignant cells are impervious to LN1 signaling. These results shed light on the crucial role of LN1 in quiescence and differentiation and how defects in the LN1/PI3K/XPO6/N-actin axis explain the loss of tissue homeostasis and growth control that contributes to malignant progression.

Indexed as

Signal TransductionActinsBreast NeoplasmsCell Line, TumorFemaleHumansKaryopherinsLamininNeoplasm ProteinsPhosphatidylinositol 3-KinasesActinsKaryopherinsLamininNeoplasm ProteinsPhosphatidylinositol 3-KinasesXPO6 protein, humanbasement membranebreast cancerexportin-6extracellular matrixlaminin-111mammary glandnuclear actinquiescence

Identifiers

PMID28591581
PMCPMC6663100
OpenAlexW2623710231

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.