Currently, one of the most disputed hypotheses regarding
breast cancer (BC) development is exposure to short wavelength artificial light at night (ALAN) as multiple studies suggest a possible link between them. This link is suggested to be mediated by nocturnal
melatonin suppression that plays an integral role in circadian regulations including cell division. The objective of the research was to evaluate effects of 1 × 30 min/midnight ALAN (134 µ Wcm-2, 460 nm) with or without nocturnal
melatonin supplement on
tumor development and epigenetic responses in 4T1
tumor-bearing BALB/c mice. Mice were monitored for body mass (Wb) and
tumor volume for 3 weeks and thereafter urine samples were collected at regular intervals for determining daily rhythms of
6-sulfatoxymelatonin (6-SMT). Finally, mice were sacrificed and the
tumor, lungs, liver, and spleen were excised for analyzing the total activity of
DNA methyltransferases (DNMT) and global DNA methylation (GDM) levels. Mice exposed to ALAN significantly reduced 6-SMT levels and increased Wb,
tumor volume, and lung
metastasis compared with controls. These effects were diminished by
melatonin. The DNMT activity and GDM levels showed tissue-specific response. The enzymatic activity and GDM levels were lower in
tumor and liver and higher in spleen and lungs under ALAN compared with controls. Our results suggest that ALAN disrupts the
melatonin rhythm and potentially leading to increased BC burden by affecting DNMT activity and GDM levels. These data may also be applicable to early detection and management of BC by monitoring
melatonin and GDM levels as early
biomarker of ALAN circadian disruption.