Second AKT: The rise of SGK in cancer signalling

Maressa Bruhn; Richard Pearson; Ross Hannan; Karen Sheppard

doi:10.3109/08977194.2010.518616

Second AKT: The rise of SGK in cancer signalling

Maressa Bruhn, Richard Pearson, Ross Hannan, Karen Sheppard

Research output: Contribution to journal › Article › peer-review

116 Citations (Scopus)

Abstract

The serum and glucocorticoid kinase (SGK) family of serine/threonine kinases consists of three isoforms, SGK-1, SGK-2 and SGK-3. This family of kinases is highly homologous to the AKT kinase family, sharing similar upstream activators and downstream targets. SGKs have been implicated in the regulation of cell growth, proliferation, survival and migration: cellular processes that are dysregulated in cancer. Furthermore, SGKs lie downstream of phosphoinositide-3-kinase (PI3Kinase) signalling and interact at various levels with RAS/RAF/ERK signalling, two pathways that are involved in promoting tumorigenesis. Recent evidence suggests that mutant PI3Kinase can induce tumorigenesis through an AKT-independent but SGK3-dependent mechanism, thus implicating SGKs as potential players in malignant transformation. Here, we will review the current state of knowledge on the regulation of the SGKs and their role in normal cell physiology and transformation with a particular focus on SGK3.

Original language	English
Pages (from-to)	394-408
Number of pages	15
Journal	Growth Factors
Volume	28
Issue number	6
DOIs	https://doi.org/10.3109/08977194.2010.518616
Publication status	Published - Dec 2010

Keywords

AKT
Cancer
MTOR
PI3Kinase
SGK

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AU - Bruhn, Maressa

AU - Pearson, Richard

AU - Hannan, Ross

AU - Sheppard, Karen

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AB - The serum and glucocorticoid kinase (SGK) family of serine/threonine kinases consists of three isoforms, SGK-1, SGK-2 and SGK-3. This family of kinases is highly homologous to the AKT kinase family, sharing similar upstream activators and downstream targets. SGKs have been implicated in the regulation of cell growth, proliferation, survival and migration: cellular processes that are dysregulated in cancer. Furthermore, SGKs lie downstream of phosphoinositide-3-kinase (PI3Kinase) signalling and interact at various levels with RAS/RAF/ERK signalling, two pathways that are involved in promoting tumorigenesis. Recent evidence suggests that mutant PI3Kinase can induce tumorigenesis through an AKT-independent but SGK3-dependent mechanism, thus implicating SGKs as potential players in malignant transformation. Here, we will review the current state of knowledge on the regulation of the SGKs and their role in normal cell physiology and transformation with a particular focus on SGK3.

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Second AKT: The rise of SGK in cancer signalling

Abstract

Keywords

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