Cancer Res. 2002; 62:3598-3602
Transactivation-deficient DN-p73 acts as an oncogene.
Stiewe T, Zimmermann S, Frilling A, Esche H, Pützer BM.
The recently discovered p53-family member p73 displays significant homology to p53, but data from primary tumors and knockout mice argue against p73 being a classical tumor suppressor. We report on the overexpression of NH(2)-terminally truncated, transactivation-deficient p73 proteins (DeltaTA-p73) in human cancer cells. Moreover, we show that DeltaTA-p73 overexpression results in malignant transformation of NIH3T3 fibroblasts and tumor growth in nude mice, thereby providing the experimental evidence for an oncogenic function of DeltaTA-p73. Apparently, increased expression of NH(2)-terminally truncated p73 isoforms conveys the TP73 gene with oncogenic activity that appears to be actively selected for during tumor development.
Contact
Institute of Experimental Gene Therapy and Cancer Research
Core-Facility Viral Vector & Genome-Editing Technologies
Biomedical Research Center
Schillingallee 69
D-18057 Rostock
Office
Ingrid Winkler
(+49) 381 494-5066(+49) 381 494-5062
ingrid.winkler@med.uni-rostock.de
Department Life, Light & Matter
Research Building LL&M
Albert-Einstein-Str. 25
D-18059 Rostock
Research Building LL&M
Albert-Einstein-Str. 25
D-18059 Rostock