Evidence map›Paper›PMID 37452991›Full record

ArticleMedical oncology (Northwood, London, England)2023

Proapoptotic and proautophagy effect of H1-receptor antagonist desloratadine in human glioblastoma cell lines.

Sasenka Vidicevic-Novakovic, Zeljka Stanojevic, Nina Tomonjic, Katarina Karapandza, Janko Zekovic, Tamara Martinovic, Danica Grujicic, Rosanda Ilic, Savo Raicevic, Jelena Tasic and 1 more

Abstract read
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In one paragraph

Article in Medical oncology (Northwood, London, England), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

4 citing papers in PubMed, 4 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. 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

11 authors at 1 institution in 2 countries.

Sasenka Vidicevic-NovakovicSchool of Medicine, Institute of Medical and Clinical Biochemistry, University of Belgrade, Belgrade, Serbia.
Zeljka StanojevicSchool of Medicine, Institute of Medical and Clinical Biochemistry, University of Belgrade, Belgrade, Serbia.
Nina TomonjicSchool of Medicine, Institute of Rheumatology, University of Belgrade, Belgrade, Serbia.
Katarina KarapandzaSchool of Medicine, Institute of Medical and Clinical Biochemistry, University of Belgrade, Belgrade, Serbia.
Janko ZekovicSchool of Medicine, Institute of Medical and Clinical Biochemistry, University of Belgrade, Belgrade, Serbia.
Tamara MartinovicSchool of Medicine, Institute of Histology and Embryology, University of Belgrade, Belgrade, Serbia.
Danica GrujicicClinic of Neurosurgery, Clinical Centre of Serbia, School of Medicine, University of Belgrade, Belgrade, Serbia.
Rosanda IlicClinic of Neurosurgery, Clinical Centre of Serbia, School of Medicine, University of Belgrade, Belgrade, Serbia.
Savo RaicevicClinic of Neurosurgery, Clinical Centre of Serbia, School of Medicine, University of Belgrade, Belgrade, Serbia.
Jelena TasicSchool of Medicine, Institute of Medical and Clinical Biochemistry, University of Belgrade, Belgrade, Serbia. jelena.tasic@med.bg.ac.rs.ORCID http://orcid.org/0000-0003-2496-0359
Aleksandra IsakovicSchool of Medicine, Institute of Medical and Clinical Biochemistry, University of Belgrade, Belgrade, Serbia.
University of Belgrade · RS

Funding

Wellcome Trust 200110
6 · The paper itself

Abstract

Glioblastomas are aggressive and usually incurable high-grade gliomas without adequate treatment. In this study, we aimed to investigate the potential of desloratadine to induce apoptosis/autophagy as genetically regulated processes that can seal cancer cell fates. All experiments were performed on U251 human glioblastoma cell line and primary human glioblastoma cell culture. Cytotoxic effect of desloratadine was investigated using MTT and CV assays, while oxidative stress, apoptosis, and autophagy were detected by flow cytometry and immunoblot. Desloratadine treatment decreased cell viability of U251 human glioblastoma cell line and primary human glioblastoma cell culture (IC50 value 50 µM) by an increase of intracellular reactive oxygen species and caspase activity. Also, desloratadine decreased the expression of main autophagy repressor mTOR and its upstream activator Akt and increased the expression of AMPK. Desloratadine exerted dual cytotoxic effect inducing both apoptosis- and mTOR/AMPK-dependent cytotoxic autophagy in glioblastoma cells and primary glioblastoma cell culture.

Indexed as

Antineoplastic AgentsGlioblastomaAMP-Activated Protein KinasesApoptosisAutophagyCell Line, TumorCell ProliferationHumansLoratadineTOR Serine-Threonine KinasesAMP-Activated Protein KinasesAntineoplastic AgentsdesloratadineLoratadineTOR Serine-Threonine KinasesApoptosisAutophagyDesloratadineGlioblastomaOxidative stress

Identifiers

PMID37452991
OpenAlexW4384407702

What OpenQuestion holds

Textmetadata
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.