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Pivotal Factors in Breast Cancer Molecular Subtypes Apoptosis Induction by ELF-EMF; Ki-67, ROS Level, HER-2, and SODs
Mohadeseh Shayeghan1,2, Fatemeh Shahriari3, Fatemeh Afroughi4
1Integrative Oncology Department, Breast Cancer Research Center, ACECR, National Cancer Institute, Tehran, Iran, acecr.ac.ir.
Background:
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.
Methods:
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.
Results:
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.
Conclusion:
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.
Insights
Extremely low-frequency electromagnetic fields (ELF-EMFs) trigger programmed cell death (PCD) in breast cancer cells by increasing reactive oxygen species (ROS). HER-2-enriched cells are most susceptible, while others utilize antioxidant genes for resistance.
Area of Science:
- Biophysics
- Cell Biology
- Cancer Research
Background:
- Extremely low-frequency electromagnetic fields (ELF-EMFs) are known to induce programmed cell death (PCD) in cancer cells via reactive oxygen species (ROS) elevation.
- However, the precise mechanisms and the role of antioxidant machinery remain under-investigated.
Purpose of the Study:
- To investigate the impact of ELF-EMF exposure on ROS levels, antioxidant gene expression, and apoptosis in diverse breast cancer subtypes.
- To explore the relationship between p53 status and cellular response to ELF-EMF.
Main Methods:
- Exposure of breast cancer cell lines (SKBR-3, MDA-MB-231, MCF-7) to ELF-EMF (1 Hz, 100 mT) for 5 days (2 h/day).
- Measurement of intracellular ROS levels using DCFH-DA.
- Assessment of apoptosis via annexin V/PI staining.
- Quantification of antioxidant gene mRNA expression (SOD1, SOD2, SOD3, GSR).
Main Results:
- ELF-EMF exposure significantly increased ROS levels in all tested cell lines, with a pronounced 5-fold increase in SKBR-3 cells.
- SKBR-3 cells exhibited substantial apoptosis induction (78%), significantly higher than MDA-MB-231 (22%) and MCF-7 (11%) cells.
- Antioxidant gene expression varied: SOD1 and SOD2 increased in MDA-MB-231; SOD1, SOD2, SOD3, and GSR increased in MCF-7, while SKBR-3 showed minimal changes.
Conclusions:
- ELF-EMF induces ROS-dependent apoptosis in a p53-independent manner, particularly in HER-2-enriched breast cancer cells (SKBR-3).
- Other subtypes, such as triple-negative breast cancer (MDA-MB-231) and luminal A (MCF-7), demonstrated resistance to ELF-EMF-induced apoptosis by upregulating antioxidant genes, notably SOD1.
