Evidence map›Paper›PMID 27468826›Full record

ArticleInvestigational new drugs2016

Molecular and cellular effects of a novel hydroxamate-based HDAC inhibitor - belinostat - in glioblastoma cell lines: a preliminary report.

Magdalena Kusaczuk, Rafał Krętowski, Anna Stypułkowska, Marzanna Cechowska-Pasko

Open access · hybridAbstract read
In one paragraph

Article in Investigational new drugs, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

17 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
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  6. GPR18-Mediated Relaxation of Human Isolated Pulmonary Arteries.International journal of molecular sciences · 2022
    Article
  7. Article
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  9. The application of histone deacetylases inhibitors in glioblastoma.Journal of experimental & clinical cancer research : CR · 2020
    Review
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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

4 authors at 1 institution in 1 country.

Magdalena KusaczukDepartment of Pharmaceutical Biochemistry, Medical University of Białystok, Mickiewicza 2A, 15-222, Białystok, Poland. mkusaczuk@wp.pl.
Rafał KrętowskiDepartment of Pharmaceutical Biochemistry, Medical University of Białystok, Mickiewicza 2A, 15-222, Białystok, Poland.
Anna StypułkowskaDepartment of Pharmaceutical Biochemistry, Medical University of Białystok, Mickiewicza 2A, 15-222, Białystok, Poland.
Marzanna Cechowska-PaskoDepartment of Pharmaceutical Biochemistry, Medical University of Białystok, Mickiewicza 2A, 15-222, Białystok, Poland.
Medical University of Białystok · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Histone deacetylase (HDAC) inhibitors are now intensively investigated as potential cytostatic agents in many malignancies. Here, we provide novel information concerning the influence of belinostat (Bel), a hydroxamate-based pan-HDAC inhibitor, on glioblastoma LN-229 and LN-18 cells. We found that LN-229 cells stimulated with 2 μmol/L of Bel for 48 h resulted in 70 % apoptosis, while equivalent treatment of LN-18 cells resulted in only 28 % apoptosis. In LN-229 cells this effect was followed by up-regulation of pro-apoptotic genes including Puma, Bim, Chop and p21. In treated LN-18 cells only p21 was markedly overexpressed. Simultaneously, LN-229 cells treated with 2 μmol/L of Bel for 48 h exhibited down-regulation of molecular chaperones GRP78 and GRP94 at the protein level. In contrast, in LN-18 cells Western blot analysis did not show any marked changes in GRP78 nor GRP94 expression. Despite noticeable overexpression of p21, there were no signs of evident G1 nor G2/M cell cycle arrest, however, the reduction in number of the S phase cells was observed in both cell lines. These results collectively suggest that Bel can be considered as potential anti-glioblastoma agent. To our knowledge this is the first report presenting the effects of belinostat treatment in glioblastoma cell lines.

Indexed as

Antineoplastic AgentsApoptosisApoptosis Regulatory ProteinsBcl-2-Like Protein 11Cell Line, TumorCell SurvivalCyclin-Dependent Kinase Inhibitor p21Endoplasmic Reticulum Chaperone BiPGene Expression Regulation, NeoplasticGlioblastomaHistone Deacetylase InhibitorsHistone DeacetylasesHumansHydroxamic AcidsProto-Oncogene ProteinsSulfonamidesAntineoplastic AgentsApoptosis Regulatory ProteinsBBC3 protein, humanBcl-2-Like Protein 11belinostatCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21DDIT3 protein, humanEndoplasmic Reticulum Chaperone BiPHistone Deacetylase InhibitorsHistone DeacetylasesHSPA5 protein, humanHydroxamic AcidsProto-Oncogene ProteinsSulfonamidesTranscription Factor CHOPApoptosisBelinostatGlioblastomaGlucose regulated proteinsHistone deacetylase inhibitors

Identifiers

PMID27468826
PMCPMC5007275
OpenAlexW2503600081

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.