Evidence map›Paper›PMID 23722546›Full record

ArticleCancer research2013

Genetic ablation of the fatty acid-binding protein FABP5 suppresses HER2-induced mammary tumorigenesis.

Liraz Levi, Glenn Lobo, Mary Kathryn Doud, Johannes von Lintig, Darcie Seachrist, Gregory P Tochtrop, Noa Noy

Open access · greenAbstract read
In one paragraph

Article in Cancer research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed, 1 pooled it
4.8field-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

66 citing papers in PubMed, 1 synthesis or guideline pooled it, 109 citations in OpenAlex.

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  9. Establishment of a Mouse Model for Porokeratosis Due to Mevalonate Diphosphate Decarboxylase Deficiency.Skin research and technology : official journal of International Society for Bioengineering and the Skin (ISBS) [and] International Society for Digital Imaging of Skin (ISDIS) [and] International Society for Skin Imaging (ISSI) · 2024
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6 more citing papers are in PubMed but not listed here.

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.

Liraz LeviDepartments of Pharmacology, Chemistry, and Nutrition, Case Western Reserve University School of Medicine, Cleveland, OH44106, USA.
Glenn Lobo
Mary Kathryn Doud
Johannes von Lintig
Darcie Seachrist
Gregory P Tochtrop
Noa Noy
University School · USCase Western Reserve University · US

Funding

FUNCTIONS OF INTRACELLULAR LIPID-BINDING PROTEINSR01DK060684 · NIDDK · CORNELL UNIVERSITY ITHACA · PI BROWN, JONATHAN MARK · 2002 to 2015
$4.3M
Training Programs in Cancer PharmacologyR25CA148052 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI NOY, NOA · 2010 to 2014
$2.1M
Triterpenoid Modulators of Inflammatory Driven CarcinogenesisR01CA157735 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI TOCHTROP, GREGORY P · 2011 to 2015
$1.5M
NUCLEAR RECEPTOR LIGAND TARGETING BY THE FATTY ACID BINDING PROTEINS: IMPLICATIONF31CA165599 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI DOUD, MARY KATHRYN · 2012 to 2015
$170k
NCI NIH HHS F31 CA165599NCI NIH HHS R01 CA157735NCI NIH HHS R25 CA148052NCI NIH HHS R25-CA148052NIDDK NIH HHS R01 DK060684
6 · The paper itself

Abstract

The fatty acid-binding protein FABP5 shuttles ligands from the cytosol to the nuclear receptor PPARβ/δ (encoded for by Pparδ), thereby enhancing the transcriptional activity of the receptor. This FABP5/PPARδ pathway is critical for induction of proliferation of breast carcinoma cells by activated epidermal growth factor receptor (EGFR). In this study, we show that FABP5 is highly upregulated in human breast cancers and we provide genetic evidence of the pathophysiologic significance of FABP5 in mammary tumorigenesis. Ectopic expression of FABP5 was found to be oncogenic in 3T3 fibroblasts where it augmented the ability of PPARδ to enhance cell proliferation, migration, and invasion. To determine whether FABP5 is essential for EGFR-induced mammary tumor growth, we interbred FABP5-null mice with MMTV-ErbB2/HER2 oncomice, which spontaneously develop mammary tumors. FABP5 ablation relieved activation of EGFR downstream effector signals, decreased expression of PPARδ target genes that drive cell proliferation, and suppressed mammary tumor development. Our findings establish that FABP5 is critical for mammary tumor development, rationalizing the development of FABP5 inhibitors as novel anticarcinogenic drugs.

Indexed as

AnimalsCell MovementErb-b2 Receptor Tyrosine KinasesFatty Acid-Binding ProteinsFemaleHumansImmunoblottingImmunohistochemistryMammary Neoplasms, ExperimentalMiceMice, Inbred C57BLMice, KnockoutNeoplasm ProteinsPPAR deltaReal-Time Polymerase Chain ReactionSignal TransductionErb-b2 Receptor Tyrosine KinasesFabp5 protein, mouseFatty Acid-Binding ProteinsNeoplasm ProteinsPPAR delta

Identifiers

PMID23722546
PMCPMC4082958
OpenAlexW1982075308

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.