Universität Rostock, 2009
Abstract: N-terminally truncated, transactivation deficient isoforms of the tumor suppressor protein p73 (deltaTAp73) act as oncogenes by functional repression of p53 and full-length p73. This study demonstrates that ectopic expression of deltaTAp73 in human melanoma cell lines results in increased invasiveness, motility, adhesion to extracellular matrix components and chemoresistance of the cells. A microarray analysis revealed a differential regulation of numerous genes that are involved in tumor progression by long term expression of deltaTAp73. The current results suggest a role for deltaTAp73 in melanoma progression.
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