Evidence map›Paper›PMID 26029857›Full record

ArticleMolecules (Basel, Switzerland)2015

Cytotoxicity of the Urokinase-Plasminogen Activator Inhibitor Carbamimidothioic Acid (4-Boronophenyl) Methyl Ester Hydrobromide (BC-11) on Triple-Negative MDA-MB231 Breast Cancer Cells.

Alessandra Longo, Mariangela Librizzi, Irina S Chuckowree, Christine B Baltus, John Spencer, Claudio Luparello

Open access · goldAbstract read
In one paragraph

Article in Molecules (Basel, Switzerland), 2015. 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
0.1field-weighted citation impact, top 48% 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, 9 citations in OpenAlex.

  1. Article
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  6. miR526b and miR655 Induce Oxidative Stress in Breast Cancer.International journal of molecular sciences · 2019
    Article
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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

6 authors at 3 institutions in 2 countries.

Alessandra LongoDipartimento di Scienze e Tecnologie Biologiche, Chimiche e Farmaceutiche (STEBICEF), Edificio 16, Università di Palermo, Viale delle Scienze, 90128 Palermo, Italy. alessandra4682@hotmail.it.
Mariangela LibrizziDipartimento di Scienze e Tecnologie Biologiche, Chimiche e Farmaceutiche (STEBICEF), Edificio 16, Università di Palermo, Viale delle Scienze, 90128 Palermo, Italy. merylib@alice.it.
Irina S ChuckowreeDepartment of Chemistry, School of Life Sciences, University of Sussex, Falmer, Brighton BN1 9QJ, UK. christine.baltus@univ-tours.fr.
Christine B BaltusSchool of Science at Medway, University of Greenwich, Chatham ME4 4TB, UK. christine.baltus@univ-tours.fr.
John SpencerDepartment of Chemistry, School of Life Sciences, University of Sussex, Falmer, Brighton BN1 9QJ, UK. christine.baltus@univ-tours.fr.
Claudio LuparelloDipartimento di Scienze e Tecnologie Biologiche, Chimiche e Farmaceutiche (STEBICEF), Edificio 16, Università di Palermo, Viale delle Scienze, 90128 Palermo, Italy. claudio.luparello@unipa.it.
University of Palermo · ITUniversity of Sussex · GBUniversity of Greenwich · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BC-11 is an easily synthesized simple thiouronium-substituted phenylboronic acid, which has been shown to be cytotoxic on triple negative MDA-MB231 breast cancer cells by inducing a perturbation of cell cycle when administered at a concentration equal to its ED50 at 72 h (117 μM). Exposure of cells to BC-11, either pre-absorbed with a soluble preparation of the N-terminal fragment of urokinase-plasminogen activator (uPa), or in co-treatment with two different EGFR inhibitors, indicated that: (i) BC-11 acts via binding to the N-terminus of the enzyme where uPa- and EGF receptor-recognizing sites are present, thereby abrogating the growth-sustaining effect resulting from receptor binding; and (ii) the co-presence of the EGFR inhibitor PD153035 potentiates BC-11's cytotoxicity. Exposure of cells to a higher concentration of BC-11 corresponding to its ED75 at 72 h (250 μM) caused additional impairment of mitochondrial activity, the production of reactive oxygen species and promotion of apoptosis. Therefore, BC-11 treatment appears to show potential for the development of this class of compounds in the prevention and/or therapy of "aggressive" breast carcinoma.

Indexed as

Antineoplastic AgentsApoptosisBoronic AcidsCell CycleCell Line, TumorCell ProliferationDrug SynergismEpithelial CellsErbB ReceptorsFemaleGene ExpressionHumansMammary Glands, HumanMitochondriaPlasminogen InactivatorsQuinazolines4-((3-bromophenyl)amino)-6,7-dimethoxyquinazolineAntineoplastic AgentsBoronic AcidsEGFR protein, humanErbB ReceptorsPlasminogen InactivatorsQuinazolinesReactive Oxygen SpeciesUrokinase-Type Plasminogen ActivatorBC-11boronic acidbreast cancercytotoxicityMDA-MB231 cellsplasminogen activator inhibitor

Identifiers

PMID26029857
PMCPMC6272237
OpenAlexW1506773937

What OpenQuestion 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 OpenQuestion graph.