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First published online December 15, 2003

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Tumour suppressor siblings cooperate

The tumour suppressor p53 exerts its effects by regulating transcription of various genes required for cell cycle control, apoptosis and DNA repair. Its close relative p73 is also a transcription factor, but some splice forms lack a transactivation domain (e.g. Np73) and thus might play an antagonistic role. The extent to which the regulatory circuits involving p53 and p73 - particularly Np73 - overlap is unclear. Sétha Douc-Rasy and co-workers have therefore examined their interplay in malignant neuroblastoma cells, in which p53 is sequestered outside the nucleus (see p. 293). Surprisingly, they observe that both full-length p53 (TAp73) and Np73 stabilize p53 protein. However, TAp73 causes p53 to return to the nucleus; Np73 does not. The authors also observe that TAp73 and Np73 have differential effects on genes downstream of p53 - TAp73 induces expression of the apoptosis protein PUMA, for example, but Np73 does not. In each of these cases, the effect requires wild-type p53. By contrast, TAp73 can stimulate synthesis of the cell cycle inhibitor p21 even when endogenous p53 is mutated. These results indicate that p73 can have p53-independent effects but that, frequently, the regulatory pathways involving the proteins overlap, and the truncated Np73 plays a repressive role.

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Differential response of p53 target genes to p73 overexpression in SH-SY5Y neuroblastoma cell line

David Goldschneider, Etienne Blanc, Gilda Raguénez, Michel Barrois, Agnès Legrand, Gwenaëlle Le Roux, Hedi Haddada, Jean Bénard, and Sétha Douc-Rasy
JCS 2004 117: 293-301. [Abstract] [Full Text]  

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in JCS Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content