Evidence map›Paper›PMID 33599853›Full record

ArticleMedical oncology (Northwood, London, England)2021

Bexarotene inhibits cell proliferation by inducing oxidative stress, DNA damage and apoptosis via PPARγ/ NF-κB signaling pathway in C6 glioma cells.

Ceyhan Hacioglu, Fatih Kar, Sedat Kacar, Varol Sahinturk, Gungor Kanbak

Open access · greenAbstract read
PubMed Publisher
In one paragraph

Article in Medical oncology (Northwood, London, England), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.8field-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

15 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
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  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. RAR-Dependent and RAR-Independent RXR Signaling in Stem-like Glioma Cells.International journal of molecular sciences · 2023
    Article
  9. Article
  10. Methanol Extract ofAntioxidants (Basel, Switzerland) · 2022
    Article
  11. Article
  12. Review
  13. Article
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  15. 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

5 authors at 3 institutions in 1 country.

Ceyhan HaciogluDepartment of Medical Biochemistry, Faculty of Medicine, Düzce University, Düzce, Turkey. ceyhanhacioglu@duzce.edu.tr.ORCID http://orcid.org/0000-0002-0993-6118
Fatih KarDepartment of Medical Services and Techniques, Vocational School of Health Services, Kütahya Health Science University, Kütahya, Turkey.
Sedat KacarDepartment of Histology and Embryology, Faculty of Medicine, Eskişehir Osmangazi University, Eskişehir, Turkey.
Varol SahinturkDepartment of Histology and Embryology, Faculty of Medicine, Eskişehir Osmangazi University, Eskişehir, Turkey.
Gungor KanbakDepartment of Medical Biochemistry, Faculty of Medicine, Eskişehir Osmangazi University, Eskişehir, Turkey.
Eskişehir Osmangazi University · TRDüzce Üniversitesi · TRSağlık Bilimleri Üniversitesi · TR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gliomas are one of the most aggressive brain tumors with a poor prognosis in the central nervous system. Bexarotene is a third-generation retinoid X receptor agonist that is promising in the treatment of both cancer and neurodegenerative diseases. In this study, we aimed to investigate the cytotoxic and anti-proliferative effects of bexarotene in C6 glioma cells through the PPARγ/NF-κB pathway. In the study, first cytotoxic bexarotene concentrations for C6 cells were detected, and then apoptosis profile, reactive oxygen species (ROS), total antioxidant (TAS), 8-hydroxy-2'-deoxyguanosine (8-OHdG) and nuclear factor-κB (NF-κB) levels in the cells were determined. In addition, peroxisome proliferator-activated receptor γ (PPARγ) mRNA expression analysis was carried out. As a result, we detected concentration- and time-dependent antiproliferative effects of bexarotene on C6 cells. We found that bexarotene treatment decreased NF-κB and TAS levels and increased PPARγ and 8-OHdG levels in C6 cells. Bexarotene enhanced PPARγ expression in a dose-dependent manner when compared to the control group (P < 0.01). Furthermore, we determined that bexarotene-induced apoptotic C6 cells enhanced through Annexin V-FITC/PI staining and caspase-3/-7 activation analyses since phosphatidylserine level on the outer surface of the cell membrane and caspase-3/-7 activities were increased in the cells treated with bexarotene. In conclusion, bexarotene treatment in C6 glioma cells could modulate apoptosis profile, DNA damage, ROS production, and reduction of TAS levels through inhibition of NF-κB by enhancing PPARγ expression.

Indexed as

DNA DamageOxidative StressAnimalsAntineoplastic AgentsApoptosisBexaroteneBrain NeoplasmsCell Line, TumorCell ProliferationGliomaNF-kappa BPPAR gammaRatsRetinoid X ReceptorsSignal TransductionAntineoplastic AgentsBexaroteneNF-kappa BPPAR gammaRetinoid X Receptors8-hydroxydeoxyguanosineApoptosisBexaroteneGliomaNF-κbOxidative stressPparγRXR

Identifiers

PMID33599853
OpenAlexW3132850554

What OpenQuestion holds

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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.