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AKT-independent PI3-K signaling in cancer – emerging role for SGK3

Authors Bruhn MA, Pearson RB, Hannan RD, Sheppard KE

Received 18 April 2013

Accepted for publication 27 May 2013

Published 26 August 2013 Volume 2013:5 Pages 281—292

DOI https://doi.org/10.2147/CMAR.S35178

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 3



Maressa A Bruhn,1,6 Richard B Pearson,1–4 Ross D Hannan,1–5 Karen E Sheppard1–3

1Division of Cancer Research, Peter MacCallum Cancer Centre, Melbourne, Victoria, Australia; 2Sir Peter MacCallum Department of Oncology, 3Department of Biochemistry and Molecular Biology, University of Melbourne, Parkville, Victoria, Australia; 4Department of Biochemistry and Molecular Biology, Monash University, Clayton, Victoria, Australia; 5School of Biomedical Sciences, University of Queensland, Brisbane, Queensland, Australia; 6School of Biological Sciences, Flinders University, Bedford Park, South Australia, Australia

Abstract: The phosphoinositide 3-kinase (PI3-K) signaling pathway plays an important role in a wide variety of fundamental cellular processes, largely mediated via protein kinase B/v-akt murine thymoma viral oncogene homolog (PKB/AKT) signaling. Given the crucial role of PI3-K/AKT signaling in regulating processes such as cell growth, proliferation, and survival, it is not surprising that components of this pathway are frequently dysregulated in cancer, making the AKT kinase family members important therapeutic targets. The large number of clinical trials currently evaluating PI3-K pathway inhibitors as a therapeutic strategy further emphasizes this. The serum- and glucocorticoid-inducible protein kinase (SGK) family is made up of three isoforms, SGK1, 2, and 3, that are PI3-K-dependent, serine/threonine kinases, with similar substrate specificity to AKT. Consequently, the SGK family also regulates similar cell processes to the AKT kinases, including cell proliferation and survival. Importantly, there is emerging evidence demonstrating that SGK3 plays a critical role in AKT-independent oncogenic signaling. This review will focus on the role of SGK3 as a key effector of AKT-independent PI3-K oncogenic signaling.

Keywords:
SGK3, AKT, PI3-kinase, mTOR, cancer


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