Evidence map›Paper›PMID 33810567›Full record

ReviewBiomolecules2021

Syndecan-4 as a Pathogenesis Factor and Therapeutic Target in Cancer.

Jessica Oyie Sousa Onyeisi, Carla Cristina Lopes, Martin Götte

Open access · goldAbstract readReview
In one paragraph

Review in Biomolecules, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

29 citing papers in PubMed, 60 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
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  6. Article
  7. Article
  8. Review
  9. Review
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  11. Review
  12. Article
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  15. Article
  16. Roles of circRNAs in regulating the tumor microenvironment.Medical oncology (Northwood, London, England) · 2023
    Review
  17. Article
  18. Syndecan-4 is a maestro of gastric cancer cell invasion and communication that underscores poor survival.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  19. Article
  20. 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

3 authors at 2 institutions in 2 countries.

Jessica Oyie Sousa OnyeisiDepartment of Gynecology and Obstetrics, University Hospital Münster, Albert-Schweitzer-Campus 1, D11, 48149 Münster, Germany.ORCID 0000-0002-0411-7826
Carla Cristina LopesDisciplina de Biologia Molecular, Departamento de Bioquímica, Universidade Federal de São Paulo, São Paulo 04039-032, Brazil.ORCID 0000-0002-0840-5702
Martin GötteDepartment of Gynecology and Obstetrics, University Hospital Münster, Albert-Schweitzer-Campus 1, D11, 48149 Münster, Germany.ORCID 0000-0003-2360-2496
University Hospital Münster · DEUniversidade Federal de São Paulo · BR

Funding

Deutscher Akademischer Austauschdienst 91782193
6 · The paper itself

Abstract

Cancer is an important cause of morbidity and mortality worldwide. Advances in research on the biology of cancer revealed alterations in several key pathways underlying tumorigenesis and provided molecular targets for developing new and improved existing therapies. Syndecan-4, a transmembrane heparan sulfate proteoglycan, is a central mediator of cell adhesion, migration and proliferation. Although several studies have demonstrated important roles of syndecan-4 in cell behavior and its interactions with growth factors, extracellular matrix (ECM) molecules and cytoskeletal signaling proteins, less is known about its role and expression in multiple cancer. The data summarized in this review demonstrate that high expression of syndecan-4 is an unfavorable biomarker for estrogen receptor-negative breast cancer, glioma, liver cancer, melanoma, osteosarcoma, papillary thyroid carcinoma and testicular, kidney and bladder cancer. In contrast, in neuroblastoma and colorectal cancer, syndecan-4 is downregulated. Interestingly, syndecan-4 expression is modulated by anticancer drugs. It is upregulated upon treatment with zoledronate and this effect reduces invasion of breast cancer cells. In our recent work, we demonstrated that the syndecan-4 level was reduced after trastuzumab treatment. Similarly, syndecan-4 levels are also reduced after panitumumab treatment. Together, the data found suggest that syndecan-4 level is crucial for understanding the changes involving in malignant transformation, and also demonstrate that syndecan-4 emerges as an important target for cancer therapy and diagnosis.

Indexed as

Antineoplastic Agents, ImmunologicalApoptosisCell AdhesionExtracellular MatrixGene Expression Regulation, NeoplasticHumansNeoplasmsRNA InterferenceSignal TransductionSyndecan-4Antineoplastic Agents, ImmunologicalSyndecan-4biomarkercancerheparan sulfatemetastasisprognosisproteoglycansignal transductionsyndecan-4

Identifiers

PMID33810567
PMCPMC8065655
OpenAlexW3146420817

What Socratic holds

Textmetadata
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 Socratic graph.