YY1 is a multifunctional transcription factor capable of either repressing or activating its target genes, depending on the cellular signals and composition of its recruited complexes. Additionally, YY1 modulates the activity and stability of its interaction proteins by mediating the post-translational modifications of these proteins. Several lines of evidence exist to suggest that YY1 acts as an oncogene in prostate cancer. First, YY1 activates the expression and function of oncogenes, while inhibiting tumor suppressor activity. Secondly, the activity of YY1 itself is promoted by oncogenes and growth factors, and inhibited by tumor suppressors. Third, YY1 is overexpressed in prostate cancers.

Epigenetics implicates reversible processes that do not involve any change of DNA sequence. In theory, simultaneously targeting several epigenetic, cancer-driving pathways should result in more efficient therapies than individually targeting each of them. Thus, if a singular regulatory protein involved in the abnormality of multiple processes contributing to malignancy is identified, therapeutic targeting of this key regulator will display a substantial impact on disease progression or reversal. To date, no YY1 gene or protein mutation has been reported in any disease. YYl's regulatory role in multiple epigenetic processes coupled with its overexpression in prostate cancer lends YY1 therapeutic potential.

Many questions remain about the role of YY1 in prostate cancer-related biological pathways, and it is likely that such a promiscuous protein has more roles in prostate oncogenesis than what are currently known. Nonetheless, present evidence suggests that YY1 exerts a predominantly oncogenic function and therapeutic targeting of YY1 may result in substantial advances in prostate cancer treatment.

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