Genetic and biochemical studies demonstrate that eIF6 controls the availability of 60S ribosomal subunits and does it in two ways. First, it regulates the biogenesis of 60S in the nucleolus through an unknown mechanism. Second, it prevents improper binding of free 60S to 40S subunits in the cytoplasm, keeping them available for translation. Total loss of eIF6 is lethal due to loss of 60S biogenesis. Fifty percent reduction of eIF6 results in impairment of growth factor-induced translation, and is accompanied by increased survival in tumor models. It is becoming increasingly clear that eIF6 levels and activity are rate-liming for tumor growth in various models. However, our understanding of the connection between eIF6 and tumorigenesis is still in its infancy. Uncovering oncogenic pathways regulating eIF6 and its downstream targets will provide further clues as to the likely role of this protein in cancer biology.
eIF6 / S. Biffo, D. Brina, S. Oliveto - In: Translation and Its Regulation in Cancer Biology and Medicine / [a cura di] A. Parsyan. - [s.l] : Springer Netherlands, 2014. - ISBN 978-94-017-9077-2. - pp. 233-240 [10.1007/978-94-017-9078-9_11]
|Parole Chiave:||Antiassociation activity; Cancer; eIF6; Phosphorylation; Protein synthesis; Ribosome; Ribosome biogenesis; Tif6; Translation; Translation initiation|
|Settore Scientifico Disciplinare:||Settore BIO/06 - Anatomia Comparata e Citologia|
|Data di pubblicazione:||2014|
|Digital Object Identifier (DOI):||http://dx.doi.org/10.1007/978-94-017-9078-9_11|
|Tipologia:||Book Part (author)|
|Appare nelle tipologie:||03 - Contributo in volume|