12 T high static magnetic field suppresses osteosarcoma cells proliferation by regulating intracellular ROS and iron status.


Journal

Experimental cell research
ISSN: 1090-2422
Titre abrégé: Exp Cell Res
Pays: United States
ID NLM: 0373226

Informations de publication

Date de publication:
15 08 2022
Historique:
received: 02 01 2022
revised: 17 05 2022
accepted: 22 05 2022
pubmed: 2 6 2022
medline: 22 6 2022
entrez: 1 6 2022
Statut: ppublish

Résumé

Many studies indicated that static magnetic fields (SMFs) have anti-cancer effects. However, effect of SMFs on cancer cells with strength exceeding 12 T are rarely reported. The intracellular iron could participate in the reactive oxygen species (ROS) production and affect cell proliferation. This study aimed to investigate the effect of 12 T high static magnetic field (HiSMF) on osteosarcoma cells and the relationship with intracellular iron. The 12 T HiSMF was generated by a superconducting magnet. The proliferation was evaluated by CCK-8 assays and cell counting. The apoptosis, cell cycle distribution, and ROS were evaluated by flow cytometry. Intracellular iron status was evaluated by atomic absorption spectroscopy and Calcein-AM/2,2'-bipyridyl. The expression of cell cycle and iron metabolism-related genes were analyzed by Western Blot. The result showed that 12 T HiSMF exposure suppressed the proliferation of osteosarcoma cell lines MNNG/HOS, U-2 OS, and MG63 via cell cycle arrest in S and G2/M. Meanwhile, 12 T HiSMF increasing intracellular ROS, and its antitumor effect was reduced by antioxidant. Furthermore, the intracellular total and free iron levels, the expression of FTH1 and DMT1 were increased by 12 HiSMF. The iron chelator (DFO) could reduce the cytotoxicity of 12 T HiSMF on osteosarcoma cells. Moreover, 12 T HiSMF could enhance the cytotoxicity of cisplatin and sorafenib in osteosarcoma cells. In Conclusion, 12 T HiSMF could suppress osteosarcoma cells proliferation via intracellular iron and ROS related cell cycle arrest, and have application potential in osteosarcoma therapy combined with sorafenib and cisplatin.

Identifiants

pubmed: 35643180
pii: S0014-4827(22)00216-6
doi: 10.1016/j.yexcr.2022.113223
pii:
doi:

Substances chimiques

Reactive Oxygen Species 0
Sorafenib 9ZOQ3TZI87
Iron E1UOL152H7
Cisplatin Q20Q21Q62J

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

113223

Informations de copyright

Copyright © 2022 Elsevier Inc. All rights reserved.

Auteurs

Shenghang Wang (S)

Department of Spine Surgery, Affiliated Longhua People's Hospital, Southern Medical University (Longhua People's Hospital), Shenzhen, China; School of Life Sciences, Northwestern Polytechnical University, Xi'an, China.

Ting Huyan (T)

School of Life Sciences, Northwestern Polytechnical University, Xi'an, China; Research & Development Institute of Northwestern Polytechnical University in Shenzhen, Shenzhen, 518057, China.

Chenge Lou (C)

School of Life Sciences, Northwestern Polytechnical University, Xi'an, China; Research & Development Institute of Northwestern Polytechnical University in Shenzhen, Shenzhen, 518057, China.

Peng Shang (P)

Research & Development Institute of Northwestern Polytechnical University in Shenzhen, Shenzhen, 518057, China. Electronic address: shangpeng@nwpu.edu.cn.

Hao Zhang (H)

Department of Spine Surgery, Affiliated Longhua People's Hospital, Southern Medical University (Longhua People's Hospital), Shenzhen, China. Electronic address: zhanghaodoctor@hotmail.com.

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Classifications MeSH