YY1 studies in the clinical applications of prostate cancer

Many biological functions of YY1 implicate its oncogenic role in human cancers. Further corroborating these observations is the frequent overexpression of YY1 in cancer cells, including prostate tumors [123]. These oncogenic properties confer YY1 with great potential as a therapeutic target in prostate cancer treatment.

YY1 antagonizes p53 function through multiple mechanisms, including facilitating Mdm2-mediated p53 ubiquitination and degradation, inhibiting p53-mediated transcription, blocking p53 acetylation, and attenuating p14ARF-mediated p53 stablization [47-49]. These suggest that p53 is a primary target of overexpressed YY1's role during prostate oncogenesis. Although p53 is most commonly deleted or mutated in prostate cancers, some tumors retain functional p53, especially at their early stages [124-126]. As a result, many tumors need to overcome p53 tumor suppression early in their cell transformation process, and it is reasonable to hypothesize that YY1 plays a role in overcoming this barrier to tumorigenesis in these developing prostate neoplasms.

YY1 is also implicated as a therapeutic target through its promotion of multiple onco-genes' function and expression. The bona fide oncogene Ezh2 has been used as a marker for aggressive prostate cancers and its overexpression is associated with decreased therapeutic efficacy [127]. Since YY1 is essential to Ezh2-mediated histone H3-K27 methylation, it is possible that YY1 augments the aberrant epigenetics in prostate cancer and contributes to tumor progression by recruiting Ezh2 to its target promoters.

The role of YY1 in prostate cancer therapies has been investigated in multiple studies. As indicated above, YY1 transcriptional activity and expression are negatively regulated by NO and rituximab. Thus, the treatment of the two anticancer drugs DETA/NONOate and rituxi-mab releases YY1-mediated repression of the death receptors Fas and DR5, and sensitizes the ligand-induced apoptosis of prostate cancer cells [111, 112].

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