The effect of hypoxia on photodynamic therapy with 5-aminolevulinic acid in malignant gliomas.


Journal

Photodiagnosis and photodynamic therapy
ISSN: 1873-1597
Titre abrégé: Photodiagnosis Photodyn Ther
Pays: Netherlands
ID NLM: 101226123

Informations de publication

Date de publication:
Dec 2022
Historique:
received: 01 06 2022
revised: 24 07 2022
accepted: 05 08 2022
pubmed: 10 8 2022
medline: 15 12 2022
entrez: 9 8 2022
Statut: ppublish

Résumé

Glioblastoma (GBM) is a high-grade, poor prognosis tumor that is resistant to standard treatment. The presence of a small number of glioma stem cells (GSCs) surviving in the harsh microenvironment is responsible for their refractoriness. This study aimed to investigate the effect of a hypoxic environment on the sensitivity of GSCs to photodynamic therapy with 5-aminolevulinic acid (ALA-PDT). Six human GSC lines, Mesenchymal types HGG13, HGG30, HGG1123, and Proneural types HGG146, HGG157, HGG528, were divided into two groups: normoxia (O Hypoxia-GSCs showed higher mRNA levels of FECH (ferrochelatase), which is required for iron synthesis to convert PpⅨ to heme, compared with Normoxia-GSCs. Flow cytometry revealed that the accumulation of PpⅨ in Hypoxia-GSCs reduced upon incubation with ALA. However, Hypoxia-GSCs showed less reduction in sensitivity to ALA-PDT than Normoxia-GSCs. Hypoxia-GSCs had lower intracellular PpⅨ accumulation than Normoxia-GSCs due to increased gene expression of FECH, and that their sensitivity to ALA-PDT was reduced less, despite accumulating lower concentrations of PpⅨ. ALA-PDT is a potentially effective therapy for hypoxia-tolerant GSCs that exist in hypoxia at 5% oxygen concentration.

Sections du résumé

BACKGROUND BACKGROUND
Glioblastoma (GBM) is a high-grade, poor prognosis tumor that is resistant to standard treatment. The presence of a small number of glioma stem cells (GSCs) surviving in the harsh microenvironment is responsible for their refractoriness. This study aimed to investigate the effect of a hypoxic environment on the sensitivity of GSCs to photodynamic therapy with 5-aminolevulinic acid (ALA-PDT).
MATERIALS AND METHODS METHODS
Six human GSC lines, Mesenchymal types HGG13, HGG30, HGG1123, and Proneural types HGG146, HGG157, HGG528, were divided into two groups: normoxia (O
RESULTS RESULTS
Hypoxia-GSCs showed higher mRNA levels of FECH (ferrochelatase), which is required for iron synthesis to convert PpⅨ to heme, compared with Normoxia-GSCs. Flow cytometry revealed that the accumulation of PpⅨ in Hypoxia-GSCs reduced upon incubation with ALA. However, Hypoxia-GSCs showed less reduction in sensitivity to ALA-PDT than Normoxia-GSCs.
CONCLUSION CONCLUSIONS
Hypoxia-GSCs had lower intracellular PpⅨ accumulation than Normoxia-GSCs due to increased gene expression of FECH, and that their sensitivity to ALA-PDT was reduced less, despite accumulating lower concentrations of PpⅨ. ALA-PDT is a potentially effective therapy for hypoxia-tolerant GSCs that exist in hypoxia at 5% oxygen concentration.

Identifiants

pubmed: 35944845
pii: S1572-1000(22)00342-8
doi: 10.1016/j.pdpdt.2022.103056
pii:
doi:

Substances chimiques

Aminolevulinic Acid 88755TAZ87
Protoporphyrins 0
Oxygen S88TT14065
Photosensitizing Agents 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

103056

Informations de copyright

Copyright © 2022. Published by Elsevier B.V.

Déclaration de conflit d'intérêts

Declaration of Competing Interest None.

Auteurs

Tomohiro Ihata (T)

Department of Neurosurgery and Endovascular Neurosurgery, Osaka Medical and Pharmaceutical University, 2-7 Daigaku-Machi, Takatsuki, Osaka 569-8686, Japan.

Naosuke Nonoguchi (N)

Department of Neurosurgery and Endovascular Neurosurgery, Osaka Medical and Pharmaceutical University, 2-7 Daigaku-Machi, Takatsuki, Osaka 569-8686, Japan. Electronic address: naosuke.nonoguchi@ompu.ac.jp.

Takahiro Fujishiro (T)

Department of Neurosurgery, Tanabe Neurosurgical Hospital, Fujiidera, Osaka, Japan.

Naoki Omura (N)

Department of Neurosurgery and Endovascular Neurosurgery, Osaka Medical and Pharmaceutical University, 2-7 Daigaku-Machi, Takatsuki, Osaka 569-8686, Japan.

Shinji Kawabata (S)

Department of Neurosurgery and Endovascular Neurosurgery, Osaka Medical and Pharmaceutical University, 2-7 Daigaku-Machi, Takatsuki, Osaka 569-8686, Japan.

Yoshinaga Kajimoto (Y)

Department of Neurosurgery and Endovascular Neurosurgery, Osaka Medical and Pharmaceutical University, 2-7 Daigaku-Machi, Takatsuki, Osaka 569-8686, Japan.

Masahiko Wanibuchi (M)

Department of Neurosurgery and Endovascular Neurosurgery, Osaka Medical and Pharmaceutical University, 2-7 Daigaku-Machi, Takatsuki, Osaka 569-8686, Japan.

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