Alternative magnetic field exposure suppresses tumor growth via metabolic reprogramming.

alternating magnetic field (AMF) glioblastoma multiforme (GBM) metabolic reprogramming mitochondria oxidative phosphorylation (OXPHOS) reactive oxygen species (ROS)

Journal

Cancer science
ISSN: 1349-7006
Titre abrégé: Cancer Sci
Pays: England
ID NLM: 101168776

Informations de publication

Date de publication:
15 Jun 2024
Historique:
revised: 23 05 2024
received: 07 02 2024
accepted: 28 05 2024
medline: 15 6 2024
pubmed: 15 6 2024
entrez: 15 6 2024
Statut: aheadofprint

Résumé

Application of physical forces, ranging from ultrasound to electric fields, is recommended in various clinical practice guidelines, including those for treating cancers and bone fractures. However, the mechanistic details of such treatments are often inadequately understood, primarily due to the absence of comprehensive study models. In this study, we demonstrate that an alternating magnetic field (AMF) inherently possesses a direct anti-cancer effect by enhancing oxidative phosphorylation (OXPHOS) and thereby inducing metabolic reprogramming. We observed that the proliferation of human glioblastoma multiforme (GBM) cells (U87 and LN229) was inhibited upon exposure to AMF within a specific narrow frequency range, including around 227 kHz. In contrast, this exposure did not affect normal human astrocytes (NHA). Additionally, in mouse models implanted with human GBM cells in the brain, daily exposure to AMF for 30 min over 21 days significantly suppressed tumor growth and prolonged overall survival. This effect was associated with heightened reactive oxygen species (ROS) production and increased manganese superoxide dismutase (MnSOD) expression. The anti-cancer efficacy of AMF was diminished by either a mitochondrial complex IV inhibitor or a ROS scavenger. Along with these observations, there was a decrease in the extracellular acidification rate (ECAR) and an increase in the oxygen consumption rate (OCR). This suggests that AMF-induced metabolic reprogramming occurs in GBM cells but not in normal cells. Our results suggest that AMF exposure may offer a straightforward strategy to inhibit cancer cell growth by leveraging oxidative stress through metabolic reprogramming.

Identifiants

pubmed: 38877783
doi: 10.1111/cas.16243
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : Japan Science and Technology Agency
ID : JPMJFR205A
Organisme : Japan Agency for Medical Research and Development
ID : 19191258
Organisme : Japan Agency for Medical Research and Development
ID : 23810577
Organisme : Japan Society for the Promotion of Science
ID : 22K06928
Organisme : Ricoh Co., Ltd.

Informations de copyright

© 2024 The Author(s). Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association.

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Auteurs

Taisuke Akimoto (T)

Department of Neurosurgery, Yokohama City University Graduate School of Medicine, Yokohama, Kanagawa, Japan.

Md Rafikul Islam (MR)

Department of Biochemistry and Molecular Biology, Winthrop P. Rockefeller Cancer Institute, University of Arkansas for Medical Sciences (UAMS), Little Rock, Arkansas, USA.

Akane Nagasako (A)

Cardiovascular Research Institute, Yokohama City University Graduate School of Medicine, Yokohama, Kanagawa, Japan.

Kazuhito Kishi (K)

Ricoh Company, Ltd., Ohta-ku, Tokyo, Japan.

Rina Nakakaji (R)

Cardiovascular Research Institute, Yokohama City University Graduate School of Medicine, Yokohama, Kanagawa, Japan.

Makoto Ohtake (M)

Department of Neurosurgery, Yokohama City University Graduate School of Medicine, Yokohama, Kanagawa, Japan.

Hisashi Hasumi (H)

Department of Urology, Yokohama City University Graduate School of Medicine, Yokohama, Kanagawa, Japan.

Takashi Yamaguchi (T)

Ricoh Company, Ltd., Ohta-ku, Tokyo, Japan.

Shigeki Yamada (S)

Department of Materials System Science, Yokohama City University Graduate School of Medicine, Yokohama, Kanagawa, Japan.

Tetsuya Yamamoto (T)

Department of Neurosurgery, Yokohama City University Graduate School of Medicine, Yokohama, Kanagawa, Japan.

Yoshihiro Ishikawa (Y)

Cardiovascular Research Institute, Yokohama City University Graduate School of Medicine, Yokohama, Kanagawa, Japan.

Masanari Umemura (M)

Cardiovascular Research Institute, Yokohama City University Graduate School of Medicine, Yokohama, Kanagawa, Japan.

Classifications MeSH