Epigenetic Modulation in Breast Cancer: From Mechanisms to Therapeutic Interventions

Breast cancer, a complex and heterogeneous disease, remains a leading cause of global cancer-related morbidity and mortality. According to the World Health Organization 2020 report, breast cancer is responsible for over 685,000 deaths. This comprehensive review explores epigenetic modifications contributing to breast cancer initiation, progression, and therapeutic interventions. Dynamic modifications in DNA methylation, histone modifications, chromatin remodelling, and non-coding RNA expression patterns characterise the epigenetic landscape of breast cancer. Aberrant DNA methylation patterns, particularly in the promoter regions of tumour suppressor genes, lead to their silencing, providing a selective advantage for breast tumour cells. Histone modifications, mediated by enzymes such as histone acetyltransferases (HATs) and histone deacetylases (HDACs), influence chromatin structure, impacting gene accessibility and transcriptional activity. Dysregulation of chromatin remodelling complexes further disrupts gene expression patterns, contributing to tumour progression. Non-coding RNAs that play crucial roles in regulatory processes, such as microRNAs (miRNAs) and long non-coding RNAs (lncRNAs), are essential in breast cancer biology. The therapeutic potential of targeting epigenetic modifications in breast cancer has gathered significant interest. DNA methylation inhibitors, histone deacetylase inhibitors, and agents targeting chromatin remodelling complexes have shown promise in preclinical and clinical settings. Additionally, identifying specific epigenetic biomarkers holds the potential for personalised therapeutic approaches. This article thoroughly analyses the relationship between epigenetics and breast cancer. Understanding the epigenetic alterations driving breast cancer offers promising avenues for developing targeted therapies, ultimately improving patient outcomes.