Evidence map›Paper›PMID 35327631›Full record

ArticleBiomolecules2022

Antagonistic L1 Adhesion Molecule Mimetic Compounds Inhibit Glioblastoma Cell Migration In Vitro.

Vini Nagaraj, Mirai Mikhail, Micol Baronio, Alessia Gatto, Ashana Nayak, Thomas Theis, Ugo Cavallaro, Melitta Schachner

Open access · goldAbstract read
In one paragraph

Article in Biomolecules, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.6field-weighted citation impact, top 37% 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

7 citing papers in PubMed, 7 citations in OpenAlex.

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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

8 authors at 2 institutions in 2 countries.

Vini NagarajKeck Center for Collaborative Neuroscience, Department of Cell Biology and Neuroscience, Rutgers, The State University of New Jersey, Piscataway, NJ 08854, USA.
Mirai MikhailKeck Center for Collaborative Neuroscience, Department of Cell Biology and Neuroscience, Rutgers, The State University of New Jersey, Piscataway, NJ 08854, USA.
Micol BaronioUnit of Gynaecological Oncology Research, European Institute of Oncology IRCSS, 20139 Milan, Italy.ORCID 0000-0001-9807-2931
Alessia GattoUnit of Gynaecological Oncology Research, European Institute of Oncology IRCSS, 20139 Milan, Italy.
Ashana NayakKeck Center for Collaborative Neuroscience, Department of Cell Biology and Neuroscience, Rutgers, The State University of New Jersey, Piscataway, NJ 08854, USA.
Thomas TheisKeck Center for Collaborative Neuroscience, Department of Cell Biology and Neuroscience, Rutgers, The State University of New Jersey, Piscataway, NJ 08854, USA.ORCID 0000-0001-5555-8501
Ugo CavallaroUnit of Gynaecological Oncology Research, European Institute of Oncology IRCSS, 20139 Milan, Italy.ORCID 0000-0002-0884-6460
Melitta SchachnerKeck Center for Collaborative Neuroscience, Department of Cell Biology and Neuroscience, Rutgers, The State University of New Jersey, Piscataway, NJ 08854, USA.
Rutgers, The State University of New Jersey · USEuropean Institute of Oncology · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cell adhesion molecule L1 is a cell surface glycoprotein that promotes neuronal cell migration, fosters regeneration after spinal cord injury and ameliorates the consequences of neuronal degeneration in mouse and zebrafish models. Counter-indicative features of L1 were found in tumor progression: the more L1 is expressed, the more tumor cells migrate and increase their metastatic potential. L1's metastatic potential is further evidenced by its promotion of epithelial-mesenchymal transition, endothelial cell transcytosis and resistance to chemo- and radiotherapy. These unfortunate features are indicated by observations that cells that normally do not express L1 are induced to express it when becoming malignant. With the aim to ameliorate the devastating functions of L1 in tumors, we designed an alternative approach to counteract tumor cell migration. Libraries of small organic compounds were screened using the ELISA competition approach similar to the one that we used for identifying L1 agonistic mimetics. Whereas in the former approach, a function-triggering monoclonal antibody was used for screening libraries, we here used the function-inhibiting monoclonal antibody 324 that reduces the migration of neurons. We now show that the L1 antagonistic mimetics anagrelide, 2-hydroxy-5-fluoropyrimidine and mestranol inhibit the migration of cultured tumor cells in an L1-dependent manner, raising hopes for therapy.

Indexed as

GlioblastomaNeural Cell Adhesion Molecule L1AnimalsAntibodies, MonoclonalCell AdhesionCell MovementMiceZebrafishAntibodies, MonoclonalNeural Cell Adhesion Molecule L1antagonist mimeticsCD171L1CAMmigrationmonoclonal L1 antibody 324small compound librariestumor progression

Identifiers

PMID35327631
PMCPMC8946856
OpenAlexW4220726129

What OpenQuestion holds

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LicenceCC BY
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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.