Evidence map›Paper›PMID 29212236›Full record

ArticleOncotarget2017

Growth differentiation factor 15 mediates epithelial mesenchymal transition and invasion of breast cancers through IGF-1R-FoxM1 signaling.

Bridgette F Peake, Siobhan M Eze, Lily Yang, Robert C Castellino, Rita Nahta

Erratum issuedOpen access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
5.5field-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

43 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.

  1. Pooled it
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  7. Article
  8. Article
  9. Mechanistic Insights into Tumorigenesis from Serum Proteins.medRxiv : the preprint server for health sciences · 2025
    Article
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  15. Macrophages as a Source and Target of GDF-15.International journal of molecular sciences · 2024
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Bridgette F PeakeMolecular & Systems Pharmacology PhD Program, Graduate Division of Biological and Biomedical Sciences, Emory University, Atlanta, GA, USA.
Siobhan M EzeDepartment of Pharmacology, School of Medicine, Emory University, Atlanta, GA, USA.
Lily YangDepartment of Surgery, School of Medicine, Emory University, Atlanta, GA, USA.
Robert C CastellinoDepartment of Pediatrics, School of Medicine, Emory University, Aflac Cancer & Blood Disorders Center, Children's Healthcare of Atlanta, Atlanta, GA, USA.
Rita NahtaMolecular & Systems Pharmacology PhD Program, Graduate Division of Biological and Biomedical Sciences, Emory University, Atlanta, GA, USA.
Emory University · USChildren's Healthcare of Atlanta · US

Funding

Graduate Training in the Pharmacological StudiesT32GM008602 · NIGMS · EMORY UNIVERSITY · PI HALL, RANDY A. · 1996 to 2021
$5.1M
Mechanisms of Herceptin resistanceR01CA157754 · NCI · EMORY UNIVERSITY · PI NAHTA, RITA · 2012 to 2016
$1.8M
Targeted Therapy of Triple Negative Breast Cancer Using Theranostic NanoparticlesR01CA154129 · NCI · EMORY UNIVERSITY · PI YANG, LILY · 2011 to 2015
$1.7M
NCI NIH HHS R01 CA154129NCI NIH HHS R01 CA157754NIGMS NIH HHS T32 GM008602
6 · The paper itself

Abstract

Expression of the inflammatory cytokine growth differentiation factor 15 (GDF15) is significantly elevated in many tumor types in association with epithelial mesenchymal transition (EMT), drug resistance, and progressive disease. However, few studies have examined GDF15 expression, signaling, or function in breast cancer. In the current study, we demonstrate that GDF15 is associated with high tumor grade, ER-negativity, and HER2 overexpression in patients with breast cancer. Stable overexpression of GDF15 upregulates expression of mesenchymal markers and transcription factors, including FoxM1, and increases cellular invasion. GDF15 stable clones and breast cancer cells stimulated with recombinant human GDF15 (rhGDF15) demonstrate activation of insulin-like growth factor-1 receptor (IGF-1R), EMT, and invasion. Pharmacologic inhibition of IGF-1R reduces GDF15-mediated EMT and invasion in stable clones, and FoxM1 knockdown rescues invasion and EMT in GDF15 stable clones and rhGDF15-stimulated cells. These data suggest that IGF-1R-FoxM1 signaling is a potential mechanism through which GDF15 drives EMT and invasion of breast cancers. Further, GDF15 knockdown significantly inhibits invasion of HER2-overexpressing and triple-negative breast cancer cells, supporting further preclinical investigation of GDF15-targeted therapies.

Indexed as

breast cancerinvasionsignaling

Identifiers

PMID29212236
PMCPMC5706882
OpenAlexW2761935983

What OpenQuestion holds

Textmetadata
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.