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J Biol Chem, Vol. 275, Issue 20, 15226-15231, May 19, 2000

Induction of Neuronal Differentiation by p73 in a Neuroblastoma Cell Line*

Vincenzo De LaurenziDagger , Giuseppe Raschellá§, Daniela BarcaroliDagger , Margherita Annicchiarico-PetruzzelliDagger , Marco RanalliDagger , Maria Valeria CataniDagger , Barbara Tanno§, Antonio Costanzo||, Massimo Levrero||, and Gerry MelinoDagger **

From the Dagger  Biochemistry Laboratory, IDI-IRCCS, c/o Department of Experimental Medicine, Tor Vergata University, Via Tor Vergata 135, 00133, the § ENEA, Section of Toxicology and Biochemical Sciences, 00060, and the || Laboratory of Gene Expression, Fondazione A. Cesalpino, University of Rome "La Sapienza," 00161 Rome, Italy

The p53-related p73 and p63 genes encode proteins that share considerable structural and functional homology with p53. Despite similarities, their deletion in mice has different outcomes, implying that the three genes may play distinct roles in vivo. Here we show that endogenous p73 levels increase in neuroblastoma cells induced to differentiate by retinoic acid and that exogenously expressed p73, but not p53, is sufficient to induce both morphological (neurite outgrowth) and biochemical (expression of neurofilaments and neural cell adhesion molecule (N-CAM); down-regulation of N-MYC and up-regulation of pRB) markers of neuronal differentiation. This activity is shared, to different extents, by all p73 isoforms, whereas the transcriptionally inactive mutants of p73 isoforms are ineffective. Conversely, blockage of endogenous p73 isoforms with a dominant negative p73 results in the abrogation of retinoid-induced N-CAM promoter-driven transcription. Our results indicate that the p73 isoforms activate a pathway that is not shared by p53 and that is required for neuroblastoma cell differentiation in vitro.

* This work was supported in part by Grant Telethon-E872 from the Associazione Italiana Ricerca Cancro (AIRC) and Ministero Universitá e Ricerca Scientifica e Technologica (MURST)-40% (to G. M.), a grant from the AIRC and MURST-40% (to M. L.), and grants from the AIRC and the Associazione Neuroblastoma (to G. R. and G. M.)The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Recipient of a fellowship from Fondazione Italiana Ricerca Cancro.

** To whom correspondence should be addressed. Tel.: 39-06-20427299; Fax: 39-06-20427290; E-mail: gerry.melino@uniroma2.it.

Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.
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