Effect of Extremely Low Frequency Magnetic Fields on Gene Expression in Human Mammary Epithelial MCF10A Cells

Abstract In a New Zealand population-based case-control study we assessed associations with occupational exposure to electric shocks, extremely low-frequency magnetic fields (ELF-MF) and motor neurone disease using job-exposure matrices to assess exposure. Participants were recruited between 2013 and 2016. Associations with ever/never, duration, and cumulative exposure were assessed using logistic regression adjusted for age, sex, ethnicity, socioeconomic status, education, smoking, alcohol consumption, sports, head or spine injury and solvents, and mutually adjusted for the other exposure. All analyses were repeated stratified by sex. An elevated risk was observed for having ever worked in a job with potential for electric shocks (odds ratio (OR)=1.35, 95% confidence interval (CI): 0.98, 1.86), with the strongest association for the highest level of exposure (OR=2.01, 95%CI: 1.31, 3.09). Analysis by duration suggested a non-linear association: risk was increased for both short-duration (<3 years) (OR= 4.69, 95%CI: 2.25, 9.77) and long-duration in a job with high level of electric shock exposure (>24 years; OR=1.88; 95%CI: 1.05, 3.36), with less pronounced associations for intermediate durations. No association with ELF-MF was found. Our findings provide support for an association between occupational exposure to electric shocks and motor neurone disease but did not show associations with exposure to work-related ELF-MF.

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Arsenic hexoxide has differential effects on cell proliferation and genome-wide gene expression in human primary mammary epithelial and MCF7 cells

Scientific Reports ◽

10.1038/s41598-021-82551-3 ◽

2021 ◽

Vol 11 (1) ◽

Cited By ~ 1

Author(s):

Donguk Kim ◽

Na Yeon Park ◽

Keunsoo Kang ◽

Stuart K. Calderwood ◽

Dong-Hyung Cho ◽

...

Keyword(s):

Gene Expression ◽

Cell Cycle ◽

Cancer Cells ◽

Mammary Epithelial ◽

Mcf7 Cells ◽

Differential Effects ◽

Cycle Arrest ◽

Genome Wide ◽

Human Mammary Epithelial ◽

Genome Wide Gene Expression

AbstractArsenic is reportedly a biphasic inorganic compound for its toxicity and anticancer effects in humans. Recent studies have shown that certain arsenic compounds including arsenic hexoxide (AS4O6; hereafter, AS6) induce programmed cell death and cell cycle arrest in human cancer cells and murine cancer models. However, the mechanisms by which AS6 suppresses cancer cells are incompletely understood. In this study, we report the mechanisms of AS6 through transcriptome analyses. In particular, the cytotoxicity and global gene expression regulation by AS6 were compared in human normal and cancer breast epithelial cells. Using RNA-sequencing and bioinformatics analyses, differentially expressed genes in significantly affected biological pathways in these cell types were validated by real-time quantitative polymerase chain reaction and immunoblotting assays. Our data show markedly differential effects of AS6 on cytotoxicity and gene expression in human mammary epithelial normal cells (HUMEC) and Michigan Cancer Foundation 7 (MCF7), a human mammary epithelial cancer cell line. AS6 selectively arrests cell growth and induces cell death in MCF7 cells without affecting the growth of HUMEC in a dose-dependent manner. AS6 alters the transcription of a large number of genes in MCF7 cells, but much fewer genes in HUMEC. Importantly, we found that the cell proliferation, cell cycle, and DNA repair pathways are significantly suppressed whereas cellular stress response and apoptotic pathways increase in AS6-treated MCF7 cells. Together, we provide the first evidence of differential effects of AS6 on normal and cancerous breast epithelial cells, suggesting that AS6 at moderate concentrations induces cell cycle arrest and apoptosis through modulating genome-wide gene expression, leading to compromised DNA repair and increased genome instability selectively in human breast cancer cells.

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