TAp73 regulates ATP7A: possible implications for ageing-related diseases.

Lopriore, Piervito 
Capitanio, Nazzareno 
Panatta, Emanuele 
Di Daniele, Nicola 
Gambacurta, Alessandra 

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The p53 family member p73 controls a wide range of cellular function. Deletion of p73 in mice results in increased tumorigenesis, infertility, neurological defects and altered immune system. Despite the extensive effort directed to define the molecular underlying mechanism of p73 function a clear definition of its transcriptional signature and the extent of overlap with the other p53 family members is still missing. Here we describe a novel TAp73 target, ATP7A a member of a large family of P-type ATPases implicated in human neurogenerative conditions and cancer chemoresistance. Modulation of TAp73 expression influences basal expression level of ATP7A in different cellular models and chromatin immunoprecipitation confirmed a physical direct binding of TAp73 on ATP7A genomic regions. Bioinformatic analysis of expression profile datasets of human lung cancer patients suggests a possible implication of TAp73/ATP7A axis in human cancer. These data provide a novel TAp73-dependent target which might have implications in ageing-related diseases such as cancer and neurodegeneration.

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ageing, cancer, copper, neurodegeneration, p53 family, Age Factors, Aging, Binding Sites, Carcinoma, Non-Small-Cell Lung, Cell Line, Tumor, Copper-Transporting ATPases, Databases, Genetic, Gene Expression Regulation, Neoplastic, Humans, Lung Neoplasms, Promoter Regions, Genetic, Signal Transduction, Tumor Protein p73
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Aging (Albany NY)
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Impact Journals, LLC
Department of Clinical & Experimental Medicine, University of Foggia, Italy 3 Department of Systems Medicine, Nephrology and Hypertension Unit, Tor Vergata University Hospital, Rome, Italy. 4 Department of Experimental Medicine and Surgery, University of Rome Tor Vergata, Italy