Evidence map›Paper›PMID 33202923›Full record

ArticleCancers2020

Two Secreted Proteoglycans, Activators of Urothelial Cell-Cell Adhesion, Negatively Contribute to Bladder Cancer Initiation and Progression.

Vasiliki Papadaki, Ken Asada, Julie K Watson, Toshiya Tamura, Alex Leung, Jack Hopkins, Margaret Dellett, Noriaki Sasai, Hongorzul Davaapil, Serena Nik-Zainal and 12 more

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2020. 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
1.3field-weighted citation impact, top 21% 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, 27 citations in OpenAlex.

  1. Article
  2. Article
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  5. Review
  6. Article
  7. Article
  8. Mechanistic Insights into Tumorigenesis from Serum Proteins.medRxiv : the preprint server for health sciences · 2025
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Tumor Suppressive Role of theJournal of personalized medicine · 2022
    Article
  16. Article
  17. Cancers · 2022
    Article
  18. Article
  19. Article
  20. Article
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

22 authors at 9 institutions in 4 countries.

Vasiliki PapadakiUCL Institute of Ophthalmology, University College London, 11-43 Bath Street, London EC1V 9EL, UK.
Ken AsadaDivision of Molecular Modification and Cancer Biology, National Cancer Center Research Institute, 5-1-1 Tsukiji, Chuo-ku, Tokyo 104-0045, Japan.ORCID 0000-0003-0548-4449
Julie K WatsonDepartment of Oncology, The Hutchison/MRC Research Centre, University of Cambridge, Hills Road, Cambridge CB2 2XZ, UK.ORCID 0000-0002-1702-6085
Toshiya TamuraUCL Institute of Ophthalmology, University College London, 11-43 Bath Street, London EC1V 9EL, UK.
Alex LeungUCL Institute of Ophthalmology, University College London, 11-43 Bath Street, London EC1V 9EL, UK.
Jack HopkinsUCL Institute of Ophthalmology, University College London, 11-43 Bath Street, London EC1V 9EL, UK.ORCID 0000-0002-9581-364X
Margaret DellettUCL Institute of Ophthalmology, University College London, 11-43 Bath Street, London EC1V 9EL, UK.
Noriaki SasaiUCL Institute of Ophthalmology, University College London, 11-43 Bath Street, London EC1V 9EL, UK.ORCID 0000-0003-0360-1138
Hongorzul DavaapilUCL Institute of Ophthalmology, University College London, 11-43 Bath Street, London EC1V 9EL, UK.
Serena Nik-ZainalMRC Cancer Unit University of Cambridge Hutchison/MRC Research Centre Box 197, Cambridge Biomedical Campus, Cambridge CB2 0XZ, UK.
Rebecca LongbottomUCL Institute of Ophthalmology, University College London, 11-43 Bath Street, London EC1V 9EL, UK.
Makoto NakakidoUCL Institute of Ophthalmology, University College London, 11-43 Bath Street, London EC1V 9EL, UK.ORCID 0000-0003-0328-9914
Ryo ToriiDepartment of Mechanical Engineering, University College London, Torrington Place, London WC1E 7JE, UK.ORCID 0000-0001-9479-8719
Abhi VeerakumarasivamDepartment of Oncology, The Hutchison/MRC Research Centre, University of Cambridge, Hills Road, Cambridge CB2 2XZ, UK.
Syuzo KanekoDivision of Molecular Modification and Cancer Biology, National Cancer Center Research Institute, 5-1-1 Tsukiji, Chuo-ku, Tokyo 104-0045, Japan.
Mandeep S SagooUCL Institute of Ophthalmology, University College London, 11-43 Bath Street, London EC1V 9EL, UK.ORCID 0000-0003-1530-3824
Gillian MurphyDepartment of Oncology, The Hutchison/MRC Research Centre, University of Cambridge, Hills Road, Cambridge CB2 2XZ, UK.
Akihisa MitaniDepartment of Respiratory Medicine, The University of Tokyo Hospital, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan.
Kohei TsumotoInstitute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan.
John D KellyDepartment of Oncology, The Hutchison/MRC Research Centre, University of Cambridge, Hills Road, Cambridge CB2 2XZ, UK.
Ryuji HamamotoDivision of Molecular Modification and Cancer Biology, National Cancer Center Research Institute, 5-1-1 Tsukiji, Chuo-ku, Tokyo 104-0045, Japan.
Shin-Ichi OhnumaUCL Institute of Ophthalmology, University College London, 11-43 Bath Street, London EC1V 9EL, UK.
University College London · GBUniversity of Cambridge · GBMoorfields Eye Hospital NHS Foundation Trust · GBRIKEN Center for Advanced Intelligence Project · JPThe University of Tokyo · JPUniversity College Hospital · GBUniversity of Tokyo Hospital · JPUniversity of Ulster · GBWellcome/MRC Cambridge Stem Cell Institute · GB

Funding

Cancer Research UK 22932Cancer Research UK 23433Cancer Research UK 23916Cancer Research UK 27815Cancer Research UK C1528/A2690
6 · The paper itself

Abstract

Osteomodulin (OMD) and proline/arginine-rich end leucine repeat protein (PRELP) are secreted extracellular matrix proteins belonging to the small leucine-rich proteoglycans family. We found that OMD and PRELP were specifically expressed in umbrella cells in bladder epithelia, and their expression levels were dramatically downregulated in all bladder cancers from very early stages and various epithelial cancers. Our in vitro studies including gene expression profiling using bladder cancer cell lines revealed that OMD or PRELP application suppressed the cancer progression by inhibiting TGF-β and EGF pathways, which reversed epithelial-mesenchymal transition (EMT), activated cell-cell adhesion, and inhibited various oncogenic pathways. Furthermore, the overexpression of OMD in bladder cancer cells strongly inhibited the anchorage-independent growth and tumorigenicity in mouse xenograft studies. On the other hand, we found that in the bladder epithelia, the knockout mice of OMD and/or PRELP gene caused partial EMT and a loss of tight junctions of the umbrella cells and resulted in formation of a bladder carcinoma in situ-like structure by spontaneous breakdowns of the umbrella cell layer. Furthermore, the ontological analysis of the expression profiling of an OMD knockout mouse bladder demonstrated very high similarity with those obtained from human bladder cancers. Our data indicate that OMD and PRELP are endogenous inhibitors of cancer initiation and progression by controlling EMT. OMD and/or PRELP may have potential for the treatment of bladder cancer.

Indexed as

bladder cancer initiationOMDpartial EMTPRELPtight junctiontumor suppression gene

Identifiers

PMID33202923
PMCPMC7697838
OpenAlexW3106197153

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.