The ubiquitous transcription factor Yin Yang 1 (YY1) is known to have a 
fundamental role in normal biologic processes such as embryogenesis, 
differentiation, replication, and cellular proliferation. YY1 exerts its effects 
on genes involved in these processes via its ability to initiate, activate, or 
repress transcription depending upon the context in which it binds. Mechanisms 
of action include direct activation or repression, indirect activation or 
repression via cofactor recruitment, or activation or repression by disruption 
of binding sites or conformational DNA changes. YY1 activity is regulated by 
transcription factors and cytoplasmic proteins that have been shown to abrogate 
or completely inhibit YY1-mediated activation or repression; however, these 
mechanisms have not yet been fully elucidated. Since expression and function of 
YY1 are known to be intimately associated with progression through phases of the 
cell cycle, the physiologic significance of YY1 activity has recently been 
applied to models of tumor biology. The majority of the data are consistent with 
the hypothesis that YY1 overexpression and/or activation is associated with 
unchecked cellular proliferation, resistance to apoptotic stimuli, tumorigenesis 
and metastatic potential. Studies involving hematopoetic tumors, 
epithelial-based tumors, endocrine organ malignancies, hepatocellular carcinoma, 
and retinoblastoma support this hypothesis. Molecular mechanisms that have been 
investigated include YY1-mediated downregulation of p53 activity, interference 
with poly-ADP-ribose polymerase, alteration in c-myc and nuclear factor-kappa B 
(NF-kappaB) expression, regulation of death genes and gene products, and 
differential YY1 binding in the presence of inflammatory mediators. Further, 
recent findings implicate YY1 in the regulation of tumor cell resistance to 
chemotherapeutics and immune-mediated apoptotic stimuli. Taken together, these 
findings provide strong support of the hypothesis that YY1, in addition to its 
regulatory roles in normal biologic processes, may possess the potential to act 
as an initiator of tumorigenesis and may thus serve as both a diagnostic and 
prognostic tumor marker; furthermore, it may provide an effective target for 
antitumor chemotherapy and/or immunotherapy.