Evidence map›Paper›PMID 26452103›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2015

Both IGF1R and INSR Knockdown Exert Antitumorigenic Effects in Prostate Cancer In Vitro and In Vivo.

Philipp Ofer, Isabel Heidegger, Iris E Eder, Bernd Schöpf, Hannes Neuwirt, Stephan Geley, Helmut Klocker, Petra Massoner

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular endocrinology (Baltimore, Md.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.6field-weighted citation impact, top 34% 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

17 citing papers in PubMed, 25 citations in OpenAlex.

  1. Trial
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  3. Conformational dynamics in insulin receptor kinase reveal a type III allosteric pocket.Protein science : a publication of the Protein Society · 2026
    Article
  4. Article
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  7. Structural Models for a Series of Allosteric Inhibitors of IGF1R Kinase.International journal of molecular sciences · 2024
    Article
  8. Structural Models for a Series of Allosteric Inhibitors of IGF1R Kinase.bioRxiv : the preprint server for biology · 2024
    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

8 authors at 1 institution in 1 country.

Philipp OferDivision of Experimental Urology (P.O., I.H., I.E.E., H.K., P.M.), Department of Urology, Medical University, 6020 Innsbruck, Austria; Division of Genetic Epidemiology (B.S.), Department of Medical Genetics, Molecular and Clinical Pharmacology, Medical University, 6020 Innsbruck, Austria; Department of Internal Medicine IV (N.H.), Medical University, 6020 Innsbruck, Austria; and Division of Molecular Pathophysiology (S.G.), Biocenter, Medical University, 6020 Innsbruck, Austria.
Isabel HeideggerDivision of Experimental Urology (P.O., I.H., I.E.E., H.K., P.M.), Department of Urology, Medical University, 6020 Innsbruck, Austria; Division of Genetic Epidemiology (B.S.), Department of Medical Genetics, Molecular and Clinical Pharmacology, Medical University, 6020 Innsbruck, Austria; Department of Internal Medicine IV (N.H.), Medical University, 6020 Innsbruck, Austria; and Division of Molecular Pathophysiology (S.G.), Biocenter, Medical University, 6020 Innsbruck, Austria.
Iris E EderDivision of Experimental Urology (P.O., I.H., I.E.E., H.K., P.M.), Department of Urology, Medical University, 6020 Innsbruck, Austria; Division of Genetic Epidemiology (B.S.), Department of Medical Genetics, Molecular and Clinical Pharmacology, Medical University, 6020 Innsbruck, Austria; Department of Internal Medicine IV (N.H.), Medical University, 6020 Innsbruck, Austria; and Division of Molecular Pathophysiology (S.G.), Biocenter, Medical University, 6020 Innsbruck, Austria.
Bernd SchöpfDivision of Experimental Urology (P.O., I.H., I.E.E., H.K., P.M.), Department of Urology, Medical University, 6020 Innsbruck, Austria; Division of Genetic Epidemiology (B.S.), Department of Medical Genetics, Molecular and Clinical Pharmacology, Medical University, 6020 Innsbruck, Austria; Department of Internal Medicine IV (N.H.), Medical University, 6020 Innsbruck, Austria; and Division of Molecular Pathophysiology (S.G.), Biocenter, Medical University, 6020 Innsbruck, Austria.
Hannes NeuwirtDivision of Experimental Urology (P.O., I.H., I.E.E., H.K., P.M.), Department of Urology, Medical University, 6020 Innsbruck, Austria; Division of Genetic Epidemiology (B.S.), Department of Medical Genetics, Molecular and Clinical Pharmacology, Medical University, 6020 Innsbruck, Austria; Department of Internal Medicine IV (N.H.), Medical University, 6020 Innsbruck, Austria; and Division of Molecular Pathophysiology (S.G.), Biocenter, Medical University, 6020 Innsbruck, Austria.
Stephan GeleyDivision of Experimental Urology (P.O., I.H., I.E.E., H.K., P.M.), Department of Urology, Medical University, 6020 Innsbruck, Austria; Division of Genetic Epidemiology (B.S.), Department of Medical Genetics, Molecular and Clinical Pharmacology, Medical University, 6020 Innsbruck, Austria; Department of Internal Medicine IV (N.H.), Medical University, 6020 Innsbruck, Austria; and Division of Molecular Pathophysiology (S.G.), Biocenter, Medical University, 6020 Innsbruck, Austria.
Helmut KlockerDivision of Experimental Urology (P.O., I.H., I.E.E., H.K., P.M.), Department of Urology, Medical University, 6020 Innsbruck, Austria; Division of Genetic Epidemiology (B.S.), Department of Medical Genetics, Molecular and Clinical Pharmacology, Medical University, 6020 Innsbruck, Austria; Department of Internal Medicine IV (N.H.), Medical University, 6020 Innsbruck, Austria; and Division of Molecular Pathophysiology (S.G.), Biocenter, Medical University, 6020 Innsbruck, Austria.
Petra MassonerDivision of Experimental Urology (P.O., I.H., I.E.E., H.K., P.M.), Department of Urology, Medical University, 6020 Innsbruck, Austria; Division of Genetic Epidemiology (B.S.), Department of Medical Genetics, Molecular and Clinical Pharmacology, Medical University, 6020 Innsbruck, Austria; Department of Internal Medicine IV (N.H.), Medical University, 6020 Innsbruck, Austria; and Division of Molecular Pathophysiology (S.G.), Biocenter, Medical University, 6020 Innsbruck, Austria.
Innsbruck Medical University · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The IGF network with its main receptors IGF receptor 1 (IGF1R) and insulin receptor (INSR) is of major importance for cancer initiation and progression. To date, clinical studies targeting this network were disappointing and call for thorough analysis of the IGF network in cancer models. We highlight the oncogenic effects controlled by IGF1R and INSR in prostate cancer cells and show similarities as well as differences after receptor knockdown (KD). In PC3 prostate cancer cells stably transduced with inducible short hairpin RNAs, targeting IGF1R or INSR attenuated cell growth and proliferation ultimately driving cells into apoptosis. IGF1R KD triggered rapid and strong antiproliferative and proapoptotic responses, whereas these effects were less pronounced and delayed after INSR KD. Down-regulation of the antiapoptotic proteins myeloid cell leukemia-1 and survivin was observed in both KDs, whereas IGF1R KD also attenuated expression of prosurvival proteins B cell lymphoma-2 and B cell lymphoma-xL. Receptor KD induced cell death involved autophagy in particular upon IGF1R KD; however, no difference in mitochondrial energy metabolism was observed. In a mouse xenograft model, induction of IGF1R or INSR KD after tumor establishment eradicated most of the tumors. After 20 days of receptor KD, tumor cells were found only in 1/14 IGF1R and 3/14 INSR KD tumor remnants. Collectively, our data underline the oncogenic functions of IGF1R and INSR in prostate cancer namely growth, proliferation, and survival in vitro as well as in vivo and identify myeloid cell leukemia-1 and survivin as important mediators of inhibitory and apoptotic effects.

Indexed as

AnimalsAntigens, CDApoptosisCell Line, TumorCell ProliferationCell SurvivalHumansMaleMiceMice, Inbred BALB CProstatic NeoplasmsReceptor, IGF Type 1Receptor, InsulinRNA, Small InterferingSignal TransductionXenograft Model Antitumor AssaysAntigens, CDINSR protein, humanReceptor, IGF Type 1Receptor, InsulinRNA, Small Interfering

Identifiers

PMID26452103
PMCPMC4669362
OpenAlexW1823708500

What OpenQuestion holds

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LicenceCC BY-NC
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.