Evidence map›Paper›PMID 28747635›Full record

ArticleNature communications2017

AIM1 is an actin-binding protein that suppresses cell migration and micrometastatic dissemination.

Michael C Haffner, David M Esopi, Alcides Chaux, Meltem Gürel, Susmita Ghosh, Ajay M Vaghasia, Harrison Tsai, Kunhwa Kim, Nicole Castagna, Hong Lam and 13 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

33 citing papers in PubMed, 46 citations in OpenAlex.

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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

23 authors at 3 institutions in 1 country.

Michael C HaffnerSidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, MD, USA.
David M EsopiSidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, MD, USA.
Alcides ChauxDepartment of Pathology, Johns Hopkins University, Baltimore, MD, USA.
Meltem GürelSidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, MD, USA.
Susmita GhoshDepartment of Pathology, Johns Hopkins University, Baltimore, MD, USA.
Ajay M VaghasiaSidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, MD, USA.
Harrison TsaiDepartment of Pathology, Johns Hopkins University, Baltimore, MD, USA.
Kunhwa KimSidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, MD, USA.
Nicole CastagnaSidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, MD, USA.
Hong LamDepartment of Environmental Health and Engineering, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD, USA.
Jessica HicksDepartment of Pathology, Johns Hopkins University, Baltimore, MD, USA.
Nicolas WyhsSidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, MD, USA.
Debika Biswal ShinoharaSidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, MD, USA.
Paula J HurleySidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, MD, USA.
Brian W SimonsBrady Urological Institute, School of Medicine, Johns Hopkins University, Baltimore, MD, USA.
Edward M SchaefferSidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, MD, USA.
Tamara L LotanDepartment of Pathology, Johns Hopkins University, Baltimore, MD, USA.
William B IsaacsSidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, MD, USA.
George J NettoSidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, MD, USA.
Angelo M De MarzoSidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, MD, USA.
William G NelsonSidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, MD, USA.
Steven S AnDepartment of Environmental Health and Engineering, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD, USA.
Srinivasan YegnasubramanianSidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, MD, USA. syegnasu@jhmi.edu.
Johns Hopkins University · USSidney Kimmel Comprehensive Cancer Center · USJohns Hopkins Medicine · US

Funding

Translational Research Central ServicesP30CA006973 · NCI · JOHNS HOPKINS UNIVERSITY · PI Rosalie Wollett · 1985 to 2026
$208.6M
TRANSGENIC MODELS FOR PROSTATE CANCER AND AUTOIMMUNITYP50CA058236 · NCI · JOHNS HOPKINS UNIVERSITY · PI DENMEADE, SAMUEL R · 1992 to 2020
$43.9M
VACCINES--A NEW PARADIGM FOR BREAST CANCERP50CA088843 · NCI · JOHNS HOPKINS UNIVERSITY · PI DAVIDSON, NANCY ELLEN · 2000 to 2010
$27.8M
The Role of Physical Cues in Collective Cell InvasionU54CA210173 · NCI · JOHNS HOPKINS UNIVERSITY · PI PIENTA, KENNETH J., WIRTZ, DENIS · 2016 to 2020
$9.9M
Multidiciplinary Integrative Genomic Approach to Distinguish Lethal from Indolent Prostate Cancer in Men of Europena and African AncestryU01CA196390 · NCI · JOHNS HOPKINS UNIVERSITY · PI DE MARZO, ANGELO MICHAEL, PIENTA, KENNETH J. · 2015 to 2020
$5.8M
GSTPI PROMOTOR HYPERMETHYLATION IN HUMAN PROSTATE CANCERR01CA070196 · NCI · JOHNS HOPKINS UNIVERSITY · PI NELSON, WILLIAM GEORGE · 1996 to 2012
$3.9M
Role of TOP2B in generating complex genomic rearrangements in human cancerR01CA183965 · NCI · JOHNS HOPKINS UNIVERSITY · PI WHEELAN, SARAH J, YEGNASUBRAMANIAN, SRINIVASAN · 2014 to 2018
$1.7M
NCI NIH HHS P30 CA006973NCI NIH HHS P50 CA058236NCI NIH HHS P50 CA088843NCI NIH HHS R01 CA070196NCI NIH HHS R01 CA183965NCI NIH HHS U01 CA196390NCI NIH HHS U54 CA210173
6 · The paper itself

Abstract

A defining hallmark of primary and metastatic cancers is the migration and invasion of malignant cells. These invasive properties involve altered dynamics of the cytoskeleton and one of its major structural components β-actin. Here we identify AIM1 (absent in melanoma 1) as an actin-binding protein that suppresses pro-invasive properties in benign prostate epithelium. Depletion of AIM1 in prostate epithelial cells increases cytoskeletal remodeling, intracellular traction forces, cell migration and invasion, and anchorage-independent growth. In addition, decreased AIM1 expression results in increased metastatic dissemination in vivo. AIM1 strongly associates with the actin cytoskeleton in prostate epithelial cells in normal tissues, but not in prostate cancers. In addition to a mislocalization of AIM1 from the actin cytoskeleton in invasive cancers, advanced prostate cancers often harbor AIM1 deletion and reduced expression. These findings implicate AIM1 as a key suppressor of invasive phenotypes that becomes dysregulated in primary and metastatic prostate cancer.

Indexed as

Cell MovementActin CytoskeletonActinsAnimalsCell LineCell Line, TumorCrystallinsHEK293 CellsHumansMaleMembrane ProteinsMiceMicroscopy, Electron, TransmissionMicroscopy, FluorescenceNeoplasm InvasivenessNeoplasm MicrometastasisActinsCRYBG1 protein, humanCrystallinsMembrane Proteins

Identifiers

PMID28747635
PMCPMC5529512
OpenAlexW2736390911

What OpenQuestion holds

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LicenceCC BY
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.