ABSTRACT
Survivin is a unique member of the inhibitor of apoptosis (IAP) protein family that interferes with postmitochondrial events, including activation of caspases. Survivin regulates the cell cycle also. It is expressed in most of the human tumors, but it is barely detectable in the terminally differentiated normal cells/tissues. Molecular mechanisms of regulation of survivin in cancer are not clearly understood. Nevertheless, the functional loss of wild-type (wt) p53 is often associated with upregulation of survivin. Tumors that overexpress survivin generally bear a poor prognosis and are associated with resistance to therapy. The differential expression of survivin in cancer versus normal tissues makes it a useful tool in cancer diagnosis and a promising therapeutic target. A growing body of literature suggests nuclear expression of survivin as a good prognostic marker. Disruption of the survivin induction pathway has resulted in an increase in apoptosis and inhibition of tumor growth.
