Evidence map›Paper›PMID 29402961›Full record

ArticleScientific reports2018

ITGB1-dependent upregulation of Caveolin-1 switches TGFβ signalling from tumour-suppressive to oncogenic in prostate cancer.

Teijo Pellinen, Sami Blom, Sara Sánchez, Katja Välimäki, John-Patrick Mpindi, Hind Azegrouz, Raffaele Strippoli, Raquel Nieto, Mariano Vitón, Irene Palacios and 10 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

21 citing papers in PubMed, 43 citations in OpenAlex.

  1. Review
  2. ODC1 Polyamine Metabolism Drives Prostate Cancer via AKT and Splicing.Journal of cellular and molecular medicine · 2026
    Article
  3. Review
  4. The role of curcumin in modulating circular RNAs and long non-coding RNAs in cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    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

20 authors at 5 institutions in 4 countries.

Teijo PellinenInstitute for Molecular Medicine Finland FIMM, University of Helsinki, Biomedicum Helsinki 2U, Tukholmankatu 8, P.O. Box 20, FI-00014, 00290, Helsinki, Finland. teijo.pellinen@helsinki.fi.
Sami BlomInstitute for Molecular Medicine Finland FIMM, University of Helsinki, Biomedicum Helsinki 2U, Tukholmankatu 8, P.O. Box 20, FI-00014, 00290, Helsinki, Finland.ORCID http://orcid.org/0000-0002-1878-8911
Sara SánchezIntegrin Signalling Lab, Cell Biology & Physiology Program; Cell & Developmental Biology Area, Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain.
Katja VälimäkiInstitute for Molecular Medicine Finland FIMM, University of Helsinki, Biomedicum Helsinki 2U, Tukholmankatu 8, P.O. Box 20, FI-00014, 00290, Helsinki, Finland.
John-Patrick MpindiInstitute for Molecular Medicine Finland FIMM, University of Helsinki, Biomedicum Helsinki 2U, Tukholmankatu 8, P.O. Box 20, FI-00014, 00290, Helsinki, Finland.
Hind AzegrouzCellomics Unit, Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC, Madrid, Spain.
Raffaele StrippoliIntegrin Signalling Lab, Cell Biology & Physiology Program; Cell & Developmental Biology Area, Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain.
Raquel NietoCellomics Unit, Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC, Madrid, Spain.
Mariano VitónCellomics Unit, Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC, Madrid, Spain.
Irene PalaciosCellomics Unit, Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC, Madrid, Spain.
Riku TurkkiInstitute for Molecular Medicine Finland FIMM, University of Helsinki, Biomedicum Helsinki 2U, Tukholmankatu 8, P.O. Box 20, FI-00014, 00290, Helsinki, Finland.ORCID http://orcid.org/0000-0002-8690-6983
Yinhai WangInstitute for Molecular Medicine Finland FIMM, University of Helsinki, Biomedicum Helsinki 2U, Tukholmankatu 8, P.O. Box 20, FI-00014, 00290, Helsinki, Finland.ORCID http://orcid.org/0000-0002-3671-4932
Miguel Sánchez-AlvarezIntegrin Signalling Lab, Cell Biology & Physiology Program; Cell & Developmental Biology Area, Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain.
Stig NordlingDepartment of Pathology, Medicum, University of Helsinki, Haartmaninkatu 3 C, 00014, Helsinki, Finland.
Anna BützowDepartment of Pathology, Medicum, University of Helsinki, Haartmaninkatu 3 C, 00014, Helsinki, Finland.
Tuomas MirttiInstitute for Molecular Medicine Finland FIMM, University of Helsinki, Biomedicum Helsinki 2U, Tukholmankatu 8, P.O. Box 20, FI-00014, 00290, Helsinki, Finland.ORCID http://orcid.org/0000-0003-0455-9891
Antti RannikkoHelsinki University and Helsinki University Hospital, Department of Urology, PL340, 00029 HUS, Helsinki, Finland.
María C MontoyaCellomics Unit, Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC, Madrid, Spain.ORCID http://orcid.org/0000-0001-8878-7028
Olli KallioniemiInstitute for Molecular Medicine Finland FIMM, University of Helsinki, Biomedicum Helsinki 2U, Tukholmankatu 8, P.O. Box 20, FI-00014, 00290, Helsinki, Finland.ORCID http://orcid.org/0000-0002-3231-0332
Miguel A Del PozoIntegrin Signalling Lab, Cell Biology & Physiology Program; Cell & Developmental Biology Area, Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain. madelpozo@cnic.es.
University of Helsinki · FISpanish National Centre for Cardiovascular Research · ESInstituto de Salud Carlos III · ESAstraZeneca (United Kingdom) · GBHelsinki University Hospital · FI

Funding

Worldwide Cancer Research 15-0404
6 · The paper itself

Abstract

Caveolin-1 (CAV1) is over-expressed in prostate cancer (PCa) and is associated with adverse prognosis, but the molecular mechanisms linking CAV1 expression to disease progression are poorly understood. Extensive gene expression correlation analysis, quantitative multiplex imaging of clinical samples, and analysis of the CAV1-dependent transcriptome, supported that CAV1 re-programmes TGFβ signalling from tumour suppressive to oncogenic (i.e. induction of SLUG, PAI-1 and suppression of CDH1, DSP, CDKN1A). Supporting such a role, CAV1 knockdown led to growth arrest and inhibition of cell invasion in prostate cancer cell lines. Rationalized RNAi screening and high-content microscopy in search for CAV1 upstream regulators revealed integrin beta1 (ITGB1) and integrin associated proteins as CAV1 regulators. Our work suggests TGFβ signalling and beta1 integrins as potential therapeutic targets in PCa over-expressing CAV1, and contributes to better understand the paradoxical dual role of TGFβ in tumour biology.

Indexed as

Gene Expression Regulation, NeoplasticAdaptor Proteins, Signal TransducingCaveolin 1Cell Line, TumorHumansIntracellular Signaling Peptides and ProteinsMaleMembrane ProteinsOncogenesPhenotypeProstatic NeoplasmsSignal TransductionTransforming Growth Factor beta1Up-RegulationAdaptor Proteins, Signal TransducingCAV1 protein, humanCaveolin 1Intracellular Signaling Peptides and ProteinsITGB1BP1 protein, humanMembrane ProteinsTGFB1 protein, humanTransforming Growth Factor beta1

Identifiers

PMID29402961
PMCPMC5799174
OpenAlexW2793865924

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.