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Signaling to the ribosome in cancer—It is more than just mTORC1
Author(s) -
Hannan Katherine M.,
Sanij Elaine,
Hein Nadine,
Hannan Ross D.,
Pearson Richard B.
Publication year - 2011
Publication title -
iubmb life
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.132
H-Index - 113
eISSN - 1521-6551
pISSN - 1521-6543
DOI - 10.1002/iub.428
Subject(s) - mtorc1 , pi3k/akt/mtor pathway , microbiology and biotechnology , ribosome , signal transduction , kinase , translation (biology) , protein kinase b , protein biosynthesis , biology , chemistry , cancer research , messenger rna , gene , rna , biochemistry
It is becoming increasingly clear that dysregulation of protein synthesis contributes to a range of diseases characterized by tissue overgrowth. These include arterial stenosis, cardiac hypertrophy, hamartomas, and cancer. The central hub for the regulation of protein synthesis is the ribosome, where the key signaling pathways downstream of RAS, MYC, and phosphatidylinositol‐3‐kinase (PI3K) converge to confer exquisite, coordinated control of ribosome synthesis and function. Such cooperation ensures strict regulation of protein synthesis rates and cell growth. This review will focus on the role the PI3K/AKT/mammalian target of rapamycin complex 1 (mTORC1) pathway plays in regulating ribosome function during both health and disease, its interaction with the other key growth regulatory pathways activated by RAS and MYC, and the therapeutic potential for targeting this network. © 2011 IUBMB IUBMB Life, 63(2): 79–85, 2011