The Neurokinin-1 Receptor Is Essential for the Viability of Human Glioma Cells: A Possible Target for Treating Glioblastoma
Muñoz MF., Argüelles S., Rosso M., Medina R., Coveñas R., Ayala A.
Prospective Study, published in Biomed Res Int (2022) — summary generated from the PubMed abstract.
Early human evidence such as case series or small samples is exploring possible benefits.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Prospective Study
- Journal
- Biomed Res Int (2022)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 35434136
- PMCID
- PMC9006081
- DOI
- 10.1155/2022/6291504
- Citations
- 23
Abstract (original English)
Background Glioblastoma or glioma is the most common malignant brain tumor. Patients have a prognosis of approximately 15 months, despite the current aggressive treatment. Neurokinin-1 receptor (NK-1R) occurs naturally in human glioma, and it is necessary for the tumor development. Objective The purpose of the study was to increase the knowledge about the involvement of the substance P (SP)/NK-1R system in human glioma. Methods Cellular localization of NK-1R and SP was studied in GAMG and U-87 MG glioma cell lines by immunofluorescence. The contribution of both SP and NK-1R to the viability of these cells was also assessed after applying the tachykinin 1 receptor ( TAC1R ) or the tachykinin 1 ( TAC1 ) small interfering RNA gene silencing method, respectively. Results Both SP and the NK-1R (full-length and truncated isoforms) were localized in the nucleus and cytoplasm of GAMG and U-87 MG glioma cells. The presence of full-length NK-1R isoform was mainly observed in the nucleus, while the level of truncated isoform was higher in the cytoplasm. Cell proliferation was decreased when glioma cells were transfected with TAC1R siRNA, but not with TAC1 . U-87 MG cells were more sensitive to the effect of the TAC1R inhibition than GAMG cells. The decrease in the number of glioma cells after silencing of the TAC1R siRNA gene was due to apoptotic and necrotic mechanisms. In human primary
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
Evidence level
Early human evidence such as case series or small samples is exploring possible benefits.
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