Evidence map›Paper›PMID 26075720›Full record

ArticlePloS one2015

Pim Kinases Promote Migration and Metastatic Growth of Prostate Cancer Xenografts.

Niina M Santio, Sini K Eerola, Ilkka Paatero, Jari Yli-Kauhaluoma, Fabrice Anizon, Pascale Moreau, Johanna Tuomela, Pirkko Härkönen, Päivi J Koskinen

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
6.0field-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

38 citing papers in PubMed, 1 synthesis or guideline pooled it, 66 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Pim Kinases: Important Regulators of Cardiovascular Disease.International journal of molecular sciences · 2023
    Review
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  19. Review
  20. The role of Pim kinase in immunomodulation.American journal of cancer research · 2020
    Review
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

9 authors at 5 institutions in 2 countries.

Niina M SantioSection of Genetics and Physiology, Department of Biology, University of Turku, 20500 Turku, Finland; Drug Research Doctoral Programme, University of Turku, 20520 Turku, Finland.
Sini K EerolaSection of Genetics and Physiology, Department of Biology, University of Turku, 20500 Turku, Finland.
Ilkka PaateroInstitute of Biomedicine, Department of Medical Biochemistry and Genetics, University of Turku, 20520 Turku, Finland.
Jari Yli-KauhaluomaDivision of Pharmaceutical Chemistry and Technology, Faculty of Pharmacy, University of Helsinki, 00014 Helsinki, Finland.
Fabrice AnizonInstitut de Chimie de Clermont-Ferrand, Université Clermont Auvergne, Université Blaise Pascal, 63000 Clermont-Ferrand, France; Centre National de la Recherche Scientifique, 63178 Aubiere, France.
Pascale MoreauInstitut de Chimie de Clermont-Ferrand, Université Clermont Auvergne, Université Blaise Pascal, 63000 Clermont-Ferrand, France; Centre National de la Recherche Scientifique, 63178 Aubiere, France.
Johanna TuomelaInstitute of Biomedicine, Department of Cell Biology and Anatomy, University of Turku, 20520 Turku, Finland; Pharmatest Services Ltd, 20520 Turku, Finland.
Pirkko HärkönenInstitute of Biomedicine, Department of Cell Biology and Anatomy, University of Turku, 20520 Turku, Finland.
Päivi J KoskinenSection of Genetics and Physiology, Department of Biology, University of Turku, 20500 Turku, Finland.
University of Turku · FIInstitut de Chimie de Clermont-Ferrand · FRPharmatest (Finland) · FIUniversité Clermont Auvergne · FRUniversity of Helsinki · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

methodsPim family proteins are oncogenic kinases implicated in several types of cancer and involved in regulation of cell proliferation, survival as well as motility. Here we have investigated the ability of Pim kinases to promote metastatic growth of prostate cancer cells in two xenograft models for human prostate cancer. We have also evaluated the efficacy of Pim-selective inhibitors to antagonize these effects.

resultsWe show here that tumorigenic growth of both subcutaneously and orthotopically inoculated prostate cancer xenografts is enhanced by stable overexpression of either Pim-1 or Pim-3. Moreover, Pim-overexpressing orthotopic prostate tumors are highly invasive and able to migrate not only to the nearby prostate-draining lymph nodes, but also into the lungs to form metastases. When the xenografted mice are daily treated with the Pim-selective inhibitor DHPCC-9, both the volumes as well as the metastatic capacity of the tumors are drastically decreased. Interestingly, the Pim-promoted metastatic growth of the orthotopic xenografts is associated with enhanced angiogenesis and lymphangiogenesis. Furthermore, forced Pim expression also increases phosphorylation of the CXCR4 chemokine receptor, which may enable the tumor cells to migrate towards tissues such as the lungs that express the CXCL12 chemokine ligand.

conclusionsOur results indicate that Pim overexpression enhances the invasive properties of prostate cancer cells in vivo. These effects can be reduced by the Pim-selective inhibitor DHPCC-9, which can reach tumor tissues without serious side effects. Thus, Pim-targeting therapies with DHPCC-9-like compounds may help to prevent progression of local prostate carcinomas to fatally metastatic malignancies.

Indexed as

AnimalsCell Line, TumorCell MovementCell ProliferationChemokine CXCL12HeterograftsHumansLymphangiogenesisMaleMiceMice, Inbred BALB CMice, NudeNeoplasm MetastasisNeoplasm TransplantationNeovascularization, PathologicProstatic NeoplasmsChemokine CXCL12CXCL12 protein, humanCXCR4 protein, humanPIM1 protein, humanPIM3 protein, humanProtein Kinase InhibitorsProtein Serine-Threonine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-pim-1proto-oncogene proteins pimReceptors, CXCR4

Identifiers

PMID26075720
PMCPMC4467846
OpenAlexW1592912859

What OpenQuestion holds

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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.