Anticancer Non-narcotic Opium Alkaloid Papaverine Suppresses Human Glioblastoma Cell Growth.


Journal

Anticancer research
ISSN: 1791-7530
Titre abrégé: Anticancer Res
Pays: Greece
ID NLM: 8102988

Informations de publication

Date de publication:
Dec 2019
Historique:
received: 26 10 2019
revised: 11 11 2019
accepted: 12 11 2019
entrez: 8 12 2019
pubmed: 8 12 2019
medline: 18 12 2019
Statut: ppublish

Résumé

Glioblastoma (GBM) is the most aggressive type of primary malignant brain tumour. The interaction between high-mobility group box 1 (HMGB1) and receptor for advanced glycation end-products (RAGE) is important for tumour cell growth. Previously, we identified an anticancer candidate, papaverine, that inhibited the HMGB1-RAGE interaction. Our study assessed the anticancer effects of papaverine alone or in combination with temozolomide on U87MG and T98G human GBM cells using clonogenicity assays, as well as in a U87MG xenograft mouse model. The radiosensitizing efficacy of papaverine was measured based on the clonogenicity of T98G cells. Papaverine significantly inhibited the clonogenicity of U87MG and T98G cells. Compared with single treatment, the combination of papaverine and temozolomide more highly suppressed the clonogenicity of T98G cells and delayed tumour growth in the U87MG xenograft mouse model. Furthermore, papaverine increased the radiosensitivity of T98G cells. Papaverine is a potential anticancer drug in GBM treatment.

Sections du résumé

BACKGROUND BACKGROUND
Glioblastoma (GBM) is the most aggressive type of primary malignant brain tumour. The interaction between high-mobility group box 1 (HMGB1) and receptor for advanced glycation end-products (RAGE) is important for tumour cell growth. Previously, we identified an anticancer candidate, papaverine, that inhibited the HMGB1-RAGE interaction.
MATERIALS AND METHODS METHODS
Our study assessed the anticancer effects of papaverine alone or in combination with temozolomide on U87MG and T98G human GBM cells using clonogenicity assays, as well as in a U87MG xenograft mouse model. The radiosensitizing efficacy of papaverine was measured based on the clonogenicity of T98G cells.
RESULTS RESULTS
Papaverine significantly inhibited the clonogenicity of U87MG and T98G cells. Compared with single treatment, the combination of papaverine and temozolomide more highly suppressed the clonogenicity of T98G cells and delayed tumour growth in the U87MG xenograft mouse model. Furthermore, papaverine increased the radiosensitivity of T98G cells.
CONCLUSION CONCLUSIONS
Papaverine is a potential anticancer drug in GBM treatment.

Identifiants

pubmed: 31810939
pii: 39/12/6743
doi: 10.21873/anticanres.13889
doi:

Substances chimiques

Antineoplastic Agents 0
HMGB1 Protein 0
HMGB1 protein, human 0
Receptor for Advanced Glycation End Products 0
Papaverine DAA13NKG2Q
Temozolomide YF1K15M17Y

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

6743-6750

Informations de copyright

Copyright© 2019, International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.

Auteurs

Mana Inada (M)

Department of Biochemistry, Faculty of Pharmaceutical Sciences, Tokyo University of Science, Noda, Japan.

Akira Sato (A)

Department of Biochemistry, Faculty of Pharmaceutical Sciences, Tokyo University of Science, Noda, Japan akirasat@rs.tus.ac.jp.

Mika Shindo (M)

Department of Biochemistry, Faculty of Pharmaceutical Sciences, Tokyo University of Science, Noda, Japan.
National Cancer Center Hospital, Tokyo, Japan.

Yohei Yamamoto (Y)

Department of Neurosurgery, Jikei University School of Medicine, Tokyo, Japan.

Yasuharu Akasaki (Y)

Department of Neurosurgery, Jikei University School of Medicine, Tokyo, Japan.

Koichi Ichimura (K)

Division of Brain Tumor Translational Research, National Cancer Center Research Institute, Tokyo, Japan.

Sei-Ichi Tanuma (SI)

Department of Biochemistry, Faculty of Pharmaceutical Sciences, Tokyo University of Science, Noda, Japan.
Department of Genomic Medicinal Science, Research Institute for Science and Technology, Organization for Research Advancement, Tokyo University of Science, Noda, Japan.

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Classifications MeSH