The TP73 gene, a member of the p53 family, due to the use of different promoters 
and alternative splicing, is transcribed into different isoforms with 
contrasting attributes and which contribute to its functional diversity. 
Considerable efforts are made to identify the functional diversity of the p73 
splicing variants during tumorigenesis. TAp73α and TAp73β isoforms have been 
shown to differentially regulate cell cycle progression, differentiation and 
apoptosis. Interestingly, a particular increase in expression of the TAp73 
isoform, in favor of the α splicing variant, has been reported in multiple 
tumour types. Here, we report a distinctive role for TAp73β isoform in the 
control of cell migration and invasion. In fact, TAp73β- dependent induction of 
p57(Kip2) expression accounted for inhibitory effects on the actin cytoskeleton 
dynamics and thereby cancer cell motility. In contrast, TAp73α is not able to 
induce p57(Kip2) expression, and exhibits a positive effect on actin 
cytoskeleton dynamics as well as cell migration and invasion. In conclusion, the 
inhibitory effect on cell migration and invasion of TAp73β would qualify this 
distinct p73 isoform as tumor suppressor gene. In contrast, the promoting effect 
of TAp73α on cell motility and invasion strengthens the potential oncogenic 
activities of this p73 isoform.