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Abstract
The mammalian target of rapamycin (mTOR) kinase is a master regulator of protein synthesis that couples nutrient sensing to cell growth, and deregulation of this pathway is associated with tumorigenesis. p53, and its less investigated family member p73, have been shown to interact closely with mTOR pathways through the transcriptional regulation of different target genes. To investigate the metabolic changes that occur upon inhibition of the mTOR pathway and the role of p73 in this response primary mouse embryonic fibroblast from control and TAp73−/− were treated with the macrocyclic lactone rapamycin. Extensive gas chromatography/mass spectrometry (GC/MS) and liquid chromatography/mass spectrometry (LC/MS/MS) analysis were used to obtain a rapamycin-dependent global metabolome profile from control or TAp73−/− cells. In total 289 metabolites involved in selective pathways were identified; 39 biochemical metabolites were found to be significantly altered, many of which are known to be associated with the cellular stress response.
Disclosure of Potential Conflicts of Interest
No potential conflicts of interest were disclosed.
Acknowledgments
This work has been supported by the Medical Research Council, UK; grants from “Alleanza contro il Cancro” (ACC12), MIUR/PRIN (20078P7T3K_001)/FIRB (RBIP06LCA9_0023, RBIP06LCA9_0C), AIRC (2008–2010_33–08) (#5471) (2011-IG11955), AIRC 5xmille (#9979), Italian Human ProteomeNet RBRN07BMCT, MIUR/PRIN (2008MRLSNZ_004), Telethon Grant (GGPO9133), to GM Research described in this article was also supported in part by Min. Salute (Ricerca oncologica 26/07) and IDI-IRCCS (RF06 c.73, RF07 c.57, RF08 c.15, RF07 c.57) to GM. Work was supported by Ministry of Education and Science of the Russian Federation (11.G34.31.0069).
Supplemental Materials
Supplemental materials may be found here: http://www.landesbioscience.com/journals/cc/article/25450
