Triple-negative breast cancer (TNBC) is a very aggressive and diverse kind of breast cancer. Drugs that target the estrogen receptor, progesterone receptor, and human epidermal growth factor receptor 2 are less effective against TNBC because it lacks steroid hormone receptors. Recent research has shown that the pathogenesis of TNBC is also associated with epigenetic markers that either activate or silence genes, including DNA methylation, histone remodeling, and noncoding RNA-mediated regulation. Therefore, TNBC patients may benefit therapeutically from epigenetic reprogramming to return these genes to their natural state of expression. Here, we elaborate on the epigenetic alterations linked to the etiology of TNBC and potential treatment options. By reversing the identified epigenetic modifications, the function of the affected genes may be restored, hence improving the treatment response.
Key words: breast cancer; DNA methylation; epigenetics; histone modification; non-coding RNA
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