Evidence map›Paper›PMID 25569803›Full record

ArticleMolecular medicine (Cambridge, Mass.)2015

Oncogenic Role of the Ec Peptide of the IGF-1Ec Isoform in Prostate Cancer.

Athanasios Armakolas, Maria Kaparelou, Andreas Dimakakos, Efstathia Papageorgiou, Nikolaos Armakolas, Athanasios Antonopoulos, Constantina Petraki, Maria Lekarakou, Pavlos Lelovas, Martha Stathaki and 6 more

Open access · goldAbstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

12 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Review
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  9. A functional study of all 40The Journal of biological chemistry · 2018
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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

16 authors at 5 institutions in 2 countries.

Athanasios ArmakolasPhysiology Laboratory, Medical School, National and Kapodistrian University of Athens, Goudi-Athens, Greece.
Maria KaparelouPhysiology Laboratory, Medical School, National and Kapodistrian University of Athens, Goudi-Athens, Greece.
Andreas DimakakosPhysiology Laboratory, Medical School, National and Kapodistrian University of Athens, Goudi-Athens, Greece.
Efstathia PapageorgiouPhysiology Laboratory, Medical School, National and Kapodistrian University of Athens, Goudi-Athens, Greece.
Nikolaos ArmakolasThird Orthopaedic Clinic, KAT General Hospital, Kifisia, Attiki, Greece.
Athanasios AntonopoulosThird Orthopaedic Clinic, KAT General Hospital, Kifisia, Attiki, Greece.
Constantina PetrakiDepartment of Pathology, Metropolitan General Hospital, Athens, Greece.
Maria LekarakouDepartment of Pathology, Metropolitan General Hospital, Athens, Greece.
Pavlos LelovasBiomedical Research Foundation Academy of Athens, Center for Experimental Surgery, Athens, Greece.
Martha StathakiPhysiology Laboratory, Medical School, National and Kapodistrian University of Athens, Goudi-Athens, Greece.
Constantinos PsarrosPhysiology Laboratory, Medical School, National and Kapodistrian University of Athens, Goudi-Athens, Greece.
Ismene DontaLaboratory for Research of the Musculoskeletal System Theodoros Garofalidis, University of Athens, KAT Hospital Kifisia, Attiki, Greece.
Panos S GalanosMolecular Carcinogenesis Group, Laboratory of Histology and Embryology, Medical School, University of Athens, Greece.
Paul MsaouelPhysiology Laboratory, Medical School, National and Kapodistrian University of Athens, Goudi-Athens, Greece.
Vassilis G GorgoulisMolecular Carcinogenesis Group, Laboratory of Histology and Embryology, Medical School, University of Athens, Greece.
Michael KoutsilierisPhysiology Laboratory, Medical School, National and Kapodistrian University of Athens, Goudi-Athens, Greece.
National and Kapodistrian University of Athens · GRGeneral Hospital of Attica · GRMetropolitan Hospital · GRAcademy of Athens · GRManchester Academic Health Science Centre · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

IGF-1 is one of the key molecules in cancer biology; however, little is known about the role of the preferential expression of the premature IGF-1 isoforms in prostate cancer. We have examined the role of the cleaved COO- terminal peptide (PEc) of the third IGF-1 isoform, IGF-1Ec, in prostate cancer. Our evidence suggests that endogenously produced PEc induces cellular proliferation in the human prostate cancer cells (PC-3) in vitro and in vivo, by activating the ERK1/2 pathway in an autocrine/paracrine manner. PEc overexpressing cells and tumors presented evidence of epithelial to mesenchymal transition, whereas the orthotopic injection of PEc-overexpressing, normal prostate epithelium cells (HPrEC) in SCID mice was associated with increased metastatic rate. In humans, the IGF-1Ec expression was detected in prostate cancer biopsies, where its expression correlates with tumor stage. Our data describes the action of PEc in prostate cancer biology and defines its potential role in tumor growth, progression and metastasis.

Indexed as

AnimalsAutocrine CommunicationBiopsyCell Line, TumorCell ProliferationDisease Models, AnimalEpithelial-Mesenchymal TransitionGene ExpressionHeterograftsHumansInsulin-Like Growth Factor IMaleMiceMice, SCIDModels, BiologicalNeoplasm MetastasisInsulin-Like Growth Factor IPeptidesProtein Isoforms

Identifiers

PMID25569803
PMCPMC4461578
OpenAlexW2395535600

What OpenQuestion holds

Textmetadata
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.