Evidence map›Paper›PMID 35281606›Full record

ArticleBioMed research international2022

The Therapeutic Potential of Aprepitant in Glioblastoma Cancer Cells through Redox Modification.

Soodabeh Rezaei, Reza Assaran Darban, Hossein Javid, Seyed Isaac Hashemy

Open access · hybridAbstract read
In one paragraph

Article in BioMed research international, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
6.0field-weighted citation impact, top 3% 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

19 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
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  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Glioma and Peptidergic Systems: Oncogenic and Anticancer Peptides.International journal of molecular sciences · 2024
    Review
  12. Role of Cannabinoids in Oral Cancer.International journal of molecular sciences · 2024
    Review
  13. Review
  14. Review
  15. Review
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  18. 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

4 authors at 2 institutions in 1 country.

Soodabeh RezaeiDepartment of Biology, Faculty of Sciences, Mashhad Branch, Islamic Azad University, Mashhad, Iran.ORCID https://orcid.org/0000-0001-9007-9725
Reza Assaran DarbanDepartment of Biology, Faculty of Sciences, Mashhad Branch, Islamic Azad University, Mashhad, Iran.ORCID https://orcid.org/0000-0001-9126-5618
Hossein JavidDepartment of Clinical Biochemistry, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.ORCID https://orcid.org/0000-0002-2248-7708
Seyed Isaac HashemyDepartment of Clinical Biochemistry, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.ORCID https://orcid.org/0000-0002-1323-5250
Islamic Azad University, Mashhad · IRMashhad University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although there is no doubt regarding the involvement of oxidative stress in the development of glioblastoma, many questions remained unanswered about signaling cascades that regulate the redox status. Given the importance of the substance P (SP)/neurokinin 1 receptor (NK1R) system in different cancers, it was of particular interest to evaluate whether the stimulation of this cascade in glioblastoma-derived U87 cells is associated with the induction of oxidative stress. Our results showed that SP-mediated activation of NK1R not only increased the intracellular levels of malondialdehyde (MDA) and reactive oxygen species (ROS) but also reduced the concentration of thiol in U87 cells. We also found that upon SP addition, there was a significant reduction in the cells' total antioxidant capacity (TAC), revealing that the SP/NK1R axis may be involved in the regulation of oxidative stress in glioblastoma cells. The significant role of SP/NK1R in triggering oxidative stress in glioblastoma has become more evident when we found that the abrogation of the axis using aprepitant reduced cell survival, probably through exerting antioxidant effects. The results showed that both MDA and ROS concentrations were significantly reduced in the presence of aprepitant, and the number of antioxidant components of the redox system increased. Overall, these findings suggest that aprepitant might exert its anticancer effect on U87 cells through shifting the balance of oxidant and antioxidant components of the redox system.

Indexed as

GlioblastomaAntioxidantsAprepitantCell Line, TumorHumansNeurokinin-1 Receptor AntagonistsOxidation-ReductionReactive Oxygen SpeciesReceptors, Neurokinin-1Substance PAntioxidantsAprepitantNeurokinin-1 Receptor AntagonistsReactive Oxygen SpeciesReceptors, Neurokinin-1Substance P

Identifiers

PMID35281606
PMCPMC8913111
OpenAlexW4214931461

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.