Defects in the spindle assembly checkpoint are thought to
be responsible for an increased rate of aneuploidization
during tumorigenesis. Despite a plethora of information
on the correlation between BUB-MAD gene expression
levels and defects in the spindle checkpoint, very little is
known about alteration of another important spindle
checkpoint protein, Cdc20, in human cancer and its role
in tumor aneuploidy. We observed overexpression of
CDC20 in several oral squamous cell carcinoma (OSCC)
cell lines and primary head and neck tumors and provide
evidence that such overexpression of CDC20 is associated
with premature anaphase promotion, resulting in mitotic
abnormalities in OSCC cell lines. We also reconstituted
the chromosomal instability phenotype in a chromosomally
stable OSCC cell line by overexpressing CDC20.
Thus, abnormalities in the cellular level of Cdc20 may
deregulate the timing of anaphase promoting complex
(APC/C) in promoting premature anaphase, which often
results in aneuploidy in the tumor cells