Second AKT: The rise of SGK in cancer signalling

被引：127

作者：

Bruhn, Maressa A. ^{[1
,4
]}

Pearson, Richard B. ^{[1
,2
,3
]}

Hannan, Ross D. ^{[1
,2
,3
]}

Sheppard, Karen E. ^{[1
,2
]}

机构：

[1] Peter MacCallum Canc Ctr, Growth Control & Differentiat Program, Melbourne, Vic 3002, Australia

[2] Univ Melbourne, Dept Biochem & Mol Biol, Parkville, Vic 3010, Australia

[3] Monash Univ, Dept Biochem & Mol Biol, Clayton, Vic 3800, Australia

[4] Flinders Univ S Australia, Sch Biol Sci, Bedford Pk, SA 5042, Australia

来源：

GROWTH FACTORS | 2010年 / 28卷 / 06期

关键词：

SGK; AKT; PI3Kinase; mTOR; cancer; GLUCOCORTICOID-INDUCIBLE KINASE; INDUCED PROTEIN-KINASE; FORKHEAD TRANSCRIPTION FACTOR; STIMULATES PROMOTER ACTIVITY; MAMMARY EPITHELIAL-CELLS; GROWTH-FACTOR RECEPTOR; PHOX HOMOLOGY DOMAIN; KAPPA-B KINASE; REGULATED KINASE; BREAST-CANCER;

D O I：

10.3109/08977194.2010.518616

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

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

引用

页码：394 / 408

页数：15

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