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Pivotal Factors in Breast Cancer Molecular Subtypes Apoptosis Induction by ELF-EMF; Ki-67, ROS Level, HER-2, and SODs.

Created on 17 Jul 2026

Authors

Mohadeseh Shayeghan, Fatemeh Shahriari, Fatemeh Afroughi, Flora Forouzesh, Mohammad Hadi Niakan, Mohammad Amin Javidi

Published in

The breast journal. Volume 2026. Issue 1. Pages e9572421.

Abstract

Although increasing research has shown that extremely low-frequency electromagnetic fields (ELF-EMFs) specifically trigger PCD through the elevation of ROS levels in cancer cells, there is no adequate evidence to determine the exact mechanisms of this phenomenon. The antioxidant machinery may play a crucial role in this area; however, this has been neglected in previous research.
The main aim of this study was to assess the effect of ELF-EMF exposure (5 days, 1 Hz, 100 mT, 2 h/day) on ROS levels, expression levels of antioxidant genes, and apoptosis induction in different breast cancer molecular subtypes with different p53 statuses.
DCFH-DA results revealed that the ROS level increased in all three cell lines (SKBR-3, MDA-MB-231, and MCF-7); this increase was much greater in SKBR-3 (up to 5-fold compared to its sham exposure). This result was concurrent with the annexin V/PI results; SKBR-3 cells showed much more apoptosis induction (about 78%), compared with the others (22% or 11% in the other two cells). On the other hand, the mRNA expression level of SOD1 and SOD2 increased significantly in the MDA-MB-231, in addition to these two genes, the expression level of SOD3 and GSR increased in the MCF-7 cells but not in the SKBR-3.
Taken together, our results confirmed that ELF-EMF induced ROS-dependent apoptosis, especially in HER-2-enriched breast cancer cells (the SKBR-3), in a p53-independent manner. Other molecular subtypes (MDA-MB-231 as TNBC, or MCF-7 as luminal A) showed resistance against the ROS level increasing and subsequent apoptosis induction by using antioxidant genes, especially SOD1.

PMID:
42467070
Bibliographic data and abstract were imported from PubMed on 17 Jul 2026.

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