AKT-independent PI3-K signaling in cancer - emerging role for SGK3
Date
2013
Authors
Bruhn, Maressa A.
Pearson, Richard B
Hannan, Ross
Sheppard, Karen E.
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Publisher
Dove Medical Press Ltd
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.
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Keywords
Keywords: messenger RNA; phosphatidylinositol 3 kinase; protein kinase B; regulator protein; serum and glucocorticoid inducible protein kinase 3; unclassified drug; cancer growth; carcinogenesis; cell migration; cell proliferation; cell survival; down regulation; g AKT; Cancer; MTOR; PI3-kinase; SGK3
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Source
Cancer Management and Research
Type
Journal article
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Open Access
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