Evidence map›Paper›PMID 32817625›Full record

ArticlePloS one2020

Down-regulation of tenascin-C inhibits breast cancer cells development by cell growth, migration, and adhesion impairment.

Dariusz Wawrzyniak, Małgorzata Grabowska, Paweł Głodowicz, Konrad Kuczyński, Bogna Kuczyńska, Agnieszka Fedoruk-Wyszomirska, Katarzyna Rolle

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

25 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
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  9. Shaping Oncogenic Microenvironments: Contribution of Fibronectin.Frontiers in cell and developmental biology · 2024
    Review
  10. The role of TNC in atherosclerosis and drug development opportunities.International journal of biological sciences · 2024
    Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Tenascin-C in fibrosis in multiple organs: Translational implications.Seminars in cell & developmental biology · 2022
    Review
  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

7 authors at 1 institution in 1 country.

Dariusz WawrzyniakDepartment of Molecular Neurooncology, Institute of Bioorganic Chemistry of the Polish Academy of Sciences, Poznan, Poland.ORCID 0000-0002-6128-5383
Małgorzata GrabowskaDepartment of Molecular Neurooncology, Institute of Bioorganic Chemistry of the Polish Academy of Sciences, Poznan, Poland.
Paweł GłodowiczDepartment of Molecular Neurooncology, Institute of Bioorganic Chemistry of the Polish Academy of Sciences, Poznan, Poland.
Konrad KuczyńskiDepartment of Molecular Neurooncology, Institute of Bioorganic Chemistry of the Polish Academy of Sciences, Poznan, Poland.
Bogna KuczyńskaDepartment of Molecular Neurooncology, Institute of Bioorganic Chemistry of the Polish Academy of Sciences, Poznan, Poland.
Agnieszka Fedoruk-WyszomirskaLaboratory of Subcellular Structures Analysis, Institute of Bioorganic Chemistry of the Polish Academy of Sciences, Poznan, Poland.
Katarzyna RolleDepartment of Molecular Neurooncology, Institute of Bioorganic Chemistry of the Polish Academy of Sciences, Poznan, Poland.
Institute of Bioorganic Chemistry, Polish Academy of Sciences · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tenascin-C (TNC) is an extracellular matrix (ECM) glycoprotein that plays an important role in cell proliferation, migration, and tumour invasion in various cancers. TNC is one of the main protein overexpressed in breast cancer, indicating a role for this ECM molecule in cancer pathology. In this study we have evaluated the TNC loss-off-function in breast cancer cells. In our approach, we used dsRNA sharing sequence homology with TNC mRNA, called ATN-RNA. We present the data showing the effects of ATN-RNA in MDA-MB-231 cells both in monolayer and three-dimensional culture. Cells treated with ATN-RNA were analyzed for phenotypic alterations in proliferation, migration, adhesion, cell cycle, multi-caspase activation and the involvement in epithelial to mesenchymal transition (EMT) processes. As complementary analysis the oncogenomic portals were used to assess the clinical implication of TNC expression on breast cancer patient's survival, showing the TNC overexpression associated with a poor survival outcome. Our approach applied first in brain tumors and then in breast cancer cell lines reveals that ATN-RNA significantly diminishes the cell proliferation, migration and additionally, reverses the mesenchymal cells phenotype to the epithelial one. Thus, TNC could be considered as the universal target in different types of tumors, where TNC overexpression is associated with poor prognosis.

Indexed as

Biomarkers, TumorBreast NeoplasmsCell AdhesionCell MovementCell ProliferationDisease-Free SurvivalEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHumansMCF-7 CellsNeoplasm InvasivenessPrognosisRNA, Double-StrandedTenascinBiomarkers, TumorRNA, Double-StrandedTenascinTNC protein, human

Identifiers

PMID32817625
PMCPMC7440653
OpenAlexW3080427227

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.