Epigenetics: A Bridge between Artificial Light at Night and Breast Cancer
Epigenetics: A Bridge between Artificial Light at Night and Breast Cancer
Hafiza Sadaf Zahra1, Asia Iqbal2, Sayyeda Hira Hassan1, Hafiz Abdullah Shakir1*, Muhammad Khan1*, Muhammad Irfan3, Chaman Ara1, Shaukat Ali4
ABSTRACT
The second most frequent cancer all over the world is breast cancer (BC). It is reported that only about 10% BC cases are attributed due to inherited genetic mutations while remaining 90% cancer cases are associated with environmental factors. Artificial light at night (ALAN) is considered one of the major environmental risk factors for breast cancer. It inhibits production of melatonin (MLT) from pineal gland which results in abnormal epigenetic changes that relates with an increased risk of BC. The most important ALAN-mediated epigenetic changes include methylation of DNA and acetylation of histone, which are significant for growth, development and progression of BC. DNA hypermethylation of promoter CpG islands inhibits transcriptional activity by methyltransferase enzyme which results in inactivation of tumor suppressor genes (TSG), while in hypomethylation, demethyltransferase enzyme causes the activation of oncogenes by promoting transcriptional activity. Contrary to DNA methylation, histone acetylation and deacetylation results in chromatin opening and closing, respectively; leading to transcriptional activation and inactivation of genes. Histone acetylation has been frequently detected in oncogenes while histone deacetylation in TSG. Collective data from various studies demonstrate that DNA hypermethylation and histone deacetylation of TSG lead to inactivation of TSG and activation of oncogenes. The purpose of this review is to discuss the evidence based relationship between ALAN and oncogenes expression through epigenetic remodeling by DNA methylation and histone acetylation.
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December 2019
Vol. 34, Iss. 2, pp. 105-238
