Evidence map›Paper›PMID 23248119›Full record

ArticleCancer research2013

Autocrine motility factor promotes HER2 cleavage and signaling in breast cancer cells.

Dhong Hyo Kho, Pratima Nangia-Makker, Vitaly Balan, Victor Hogan, Larry Tait, Yi Wang, Avraham Raz

Abstract 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 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

24 citing papers in PubMed, 39 citations in OpenAlex.

  1. Beyond the gap: moonlighting functions of connexins in cancer.Cell communication and signaling : CCS · 2026
    Review
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  5. The Metabolite Saccharopine Impairs Neuronal Development by Inhibiting the Neurotrophic Function of Glucose-6-Phosphate Isomerase.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
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  13. Association between autocrine motility factor receptor gene polymorphism (rs2440472, rs373191257) and glioblastoma multiform in a representative Iranian population.Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences · 2018
    Article
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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

7 authors at 2 institutions in 1 country.

Dhong Hyo KhoDepartments of Oncology and Pathology, Wayne State University School of Medicine, Karmanos Cancer Institute, 110 E Warren Ave., Detroit, MI 48201, USA.
Pratima Nangia-Makker
Vitaly Balan
Victor Hogan
Larry Tait
Yi Wang
Avraham Raz
Wayne State University · USThe Barbara Ann Karmanos Cancer Institute · US

Funding

Tumor Biology and Microenvironment (Program 1)P30CA022453 · NCI · WAYNE STATE UNIVERSITY · PI PAUL M STEMMER · 1985 to 2026
$68.4M
MOTILITY FACTOR RECEPTORR01CA051714 · NCI · WAYNE STATE UNIVERSITY · PI RAZ, AVRAHAM · 1991 to 2012
$3.8M
NCI NIH HHS P30 CA022453NCI NIH HHS R01 CA051714NCI NIH HHS R01 CA51714
6 · The paper itself

Abstract

Trastuzumab (Herceptin) is an effective targeted therapy in HER2-overexpressing human breast carcinoma. However, many HER2-positive patients initially or eventually become resistant to this treatment, so elucidating mechanisms of trastuzumab resistance that emerge in breast carcinoma cells is clinically important. Here, we show that autocrine motility factor (AMF) binds to HER2 and induces cleavage to the ectodomain-deleted and constitutively active form p95HER2. Mechanistic investigations indicated that interaction of AMF with HER2 triggers HER2 phosphorylation and metalloprotease-mediated ectodomain shedding, activating phosphoinositide-3-kinase (PI3K) and mitogen-activated protein kinase signaling and ablating the ability of trastuzumab to inhibit breast carcinoma cell growth. Furthermore, we found that HER2 expression and AMF secretion were inversely related in breast carcinoma cells. On the basis of this evidence that AMF may contribute to HER2-mediated breast cancer progression, our findings suggest that AMF-HER2 interaction might be a novel target for therapeutic management of patients with breast cancer, whose disease is resistant to trastuzumab.

Indexed as

Signal TransductionAntibodies, Monoclonal, HumanizedAntineoplastic AgentsBlotting, WesternBreast NeoplasmsCell Line, TumorCell MovementCell ProliferationDrug Resistance, NeoplasmEnzyme ActivationErb-b2 Receptor Tyrosine KinasesFemaleGlucose-6-Phosphate IsomeraseHEK293 CellsHumansMitogen-Activated Protein KinasesAMFR protein, humanAntibodies, Monoclonal, HumanizedAntineoplastic AgentsErb-b2 Receptor Tyrosine KinasesGlucose-6-Phosphate IsomeraseMitogen-Activated Protein KinasesPhosphatidylinositol 3-KinasesReceptors, Autocrine Motility FactorTrastuzumab

Identifiers

PMID23248119
PMCPMC3577983
OpenAlexW2162484257

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.