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In Vitro and Vivo Study of Osteogenic PEMF Breast Lung Cancer

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Publication Title | In Vitro and Vivo Study of Osteogenic PEMF Breast Lung Cancer

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Original Article
In Vitro and in Vivo Study of the Effect of Osteogenic Pulsed Electromagnetic Fields on Breast and Lung Cancer Cells
Mike Y. Chen, MD, PhD1, Jing Li, MD1, Nianli Zhang, PhD2,
Erik I. Waldorff, PhD2, James T. Ryaby, PhD2, Philip Fedor, PhD1, Yongsheng Jia, MD1, and Yujun Wang, PhD1
Technology in Cancer Research & Treatment
Volume 21: 1-13
© The Author(s) 2022
Article reuse guidelines: DOI: 10.1177/15330338221124658
Introduction: Although there have been significant advances in research and treatments over the past decades, cancer remains a leading cause of morbidity and mortality, mostly due to resistance to standard therapies. Pulsed electromagnetic field (PEMF), a newly emerged therapeutic strategy, has been highly regarded as less invasive and almost safe to patients, is now a clinically accepted form to treat diseases including cancer. Breast and lung cancer are the most prevalent forms of human cancers, yet reported investigations on exploring regimes including PEMF are limited. Methods: Intended to examine the anti-tumor effects of a clinically accepted osteo- genic PEMF and the possibility of including PEMF in breast and lung cancer treatments, we studied the effects of 2 PEMF signals (PMF1 and PMF2) on breast and lung cancer cell growth and proliferation, as well as the possible underline mechanisms in vitro and in vivo. Results: We found that both signals caused modest but significant growth inhibition (∼5%) in MCF-7 and A549 cancer cells. Interestingly, mice xenograft tumors with A549 cells treated by PEMF were smaller in sizes than controls. However, for mice with MCF-7 tumor implants, treatment with PMF1 resulted in a slight increase (2.8%) in mean tumor size, while PMF2 treated tumors showed a 9% reduction in average size. Furthermore, PEMF increased caspase 3/7 expression levels and percentage of annexin stained cells, indicating the induction of apoptosis. It also increased G0 by 8.5%, caused changes in the expression of genes associated with cell growth suppression, DNA damage, cell cycle arrest, and apoptosis. When cancer cells or xenograft tumors treated with combined PEMF and chemotherapy drugs, PEMF showed growth inhibition effect independent of cisplatin in A549 cells, but with added effect by pemetrexed for the inhibition of MCF-7 growth. Conclusion: Together, our data suggested that clinically used osteogenic PEMF sig- nals moderately suppressed cancer cell growth and proliferation both in vitro and in vivo.
PEMF, chemotherapy drugs, tumor cell, growth, inhibition
ATCC, American Type Culture Collection; ANOVA, Analysis of variance; DAPI, 4′,6-diamidino-2-phenylindole; DMSO, Dimethyl sulfoxide; DNA, deoxyribonucleic acid; FDA, Food and Drug Administration; FITC, Fluorescein isothiocyanate; GAPDH, Glyceraldehyde 3-phosphate dehydrogenase; GFP, green fluorescent protein; LC3B, light chain 3B; MTT, 3-(4,5- dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide; PCNA, Proliferating cell nuclear antigen; PEMF, Pulsed Electric Magnetic fields; qRT-PCR, quantitative real-time polymerase chain reaction; STDEV, standard deviation; RNA, Ribonucleic acid; Names of cell lines: MCF-7, A549 MDA-MB-435, MDA-MB-231, SU-DHL-4 B-cell lymphoma.
Received: January 26, 2022; Revised: July 14, 2022; Accepted: August 18, 2022.
Despite decades of advancements in surgery, systemic thera- pies, and radiation therapy, cancer remains a leading cause of morbidity and death due to largely resistance to standard therapies caused by metastasis and recurrence. Alternative modalities are therefore being investigated to enhance the safety and efficacy of anti-cancer therapies. One innovative
1Division of Neurosurgery, City of Hope National Medical Center, Duarte, CA, USA
2Orthofix Medical Inc., Lewisville, TX, USA
Corresponding Author:
Mike Y. Chen, Division of Neurosurgery, City of Hope National Medical Center, Duarte, CA, 91010, USA.
Creative Commons Non Commercial CC BY-NC: This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License ( which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access page (

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