Evidence map›Paper›PMID 25967390›Full record

ReviewGene2015

Preclinical and clinical studies of the NEDD9 scaffold protein in cancer and other diseases.

Elena Shagisultanova, Anna V Gaponova, Rashid Gabbasov, Emmanuelle Nicolas, Erica A Golemis

Abstract readReview
In one paragraph

Review in Gene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
5.5field-weighted citation impact, top 3% 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

51 citing papers in PubMed, 98 citations in OpenAlex.

  1. Article
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  9. Non-Muscle Myosin II A: Friend or Foe in Cancer?International journal of molecular sciences · 2024
    Review
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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

5 authors at 2 institutions in 2 countries.

Elena ShagisultanovaProgram in Molecular Therapeutics, Fox Chase Cancer Center, Philadelphia, PA 19111, USA; Department of Medical Oncology, Fox Chase Cancer Center, Philadelphia, PA 19111, USA.
Anna V GaponovaProgram in Molecular Therapeutics, Fox Chase Cancer Center, Philadelphia, PA 19111, USA.
Rashid GabbasovProgram in Molecular Therapeutics, Fox Chase Cancer Center, Philadelphia, PA 19111, USA; Department of Genetics, Kazan Federal University (Volga Region), Kazan, Tatarstan, Russia.
Emmanuelle NicolasProgram in Molecular Therapeutics, Fox Chase Cancer Center, Philadelphia, PA 19111, USA.
Erica A GolemisProgram in Molecular Therapeutics, Fox Chase Cancer Center, Philadelphia, PA 19111, USA. Electronic address: Erica.Golemis@fccc.edu.
Fox Chase Cancer Center · USKazan Federal University · RU

Funding

WORD PROCESSING CENTER--COREP30CA006927 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI Eric Andrew Ross · 1985 to 2026
$138.8M
BioGPS: Extensible Web 2.0 gene portal for structured and unstructured annotationR01GM083924 · NIGMS · SCRIPPS RESEARCH INSTITUTE, THE · PI SU, ANDREW I, WU, CHUNLEI · 2008 to 2021
$5.6M
The Gene Wiki: Community intelligence applied to gene annotationR01GM089820 · NIGMS · SCRIPPS RESEARCH INSTITUTE, THE · PI SU, ANDREW I · 2010 to 2021
$5.2M
A Role for AMH Autocrine Signaling in NSCLCR21CA181287 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI GOLEMIS, ERICA A. · 2014 to 2015
$421k
NCI NIH HHS CA06927NCI NIH HHS P30 CA006927NCI NIH HHS R21 CA181287NIGMS NIH HHS GM089820NIGMS NIH HHS R01 GM083924
6 · The paper itself

Abstract

Cancer progression requires a significant reprogramming of cellular signaling to support the essential tumor-specific processes that include hyperproliferation, invasion (for solid tumors) and survival of metastatic colonies. NEDD9 (also known as CasL and HEF1) encodes a multi-domain scaffolding protein that assembles signaling complexes regulating multiple cellular processes relevant to cancer. These include responsiveness to signals emanating from the T and B cell receptors, integrins, chemokine receptors, and receptor tyrosine kinases, as well as cytoplasmic oncogenes such as BCR-ABL and FAK- and SRC-family kinases. Downstream, NEDD9 regulation of partners including CRKL, WAVE, PI3K/AKT, ERK, E-cadherin, Aurora-A (AURKA), HDAC6, and others allow NEDD9 to influence functions as pleiotropic as migration, invasion, survival, ciliary resorption, and mitosis. In this review, we summarize a growing body of preclinical and clinical data that indicate that while NEDD9 is itself non-oncogenic, changes in expression of NEDD9 (most commonly elevation of expression) are common features of tumors, and directly impact tumor aggressiveness, metastasis, and response to at least some targeted agents inhibiting NEDD9-interacting proteins. These data strongly support the relevance of further development of NEDD9 as a biomarker for therapeutic resistance. Finally, we briefly discuss emerging evidence supporting involvement of NEDD9 in additional pathological conditions, including stroke and polycystic kidney disease.

Indexed as

Adaptor Proteins, Signal TransducingHumansNeoplasmsPhosphoproteinsPolycystic Kidney DiseasesStrokeAdaptor Proteins, Signal TransducingNEDD9 protein, humanPhosphoproteinsCAS family proteinCAS-LHEF1Human malignancyNEDD9PrognosisProtein functionSignal transduction

Identifiers

PMID25967390
PMCPMC4458429
OpenAlexW650407107

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.