PI3K-independent AKT activation in cancers: a treasure trove for novel therapeutics.
PI3K-independent AKT activation in cancers: a treasure trove for novel therapeutics.
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DOI：
10.1002/jcp.24065
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发表时间：
2012-09
影响因子：
5.6
通讯作者：
Mahajan, Nupam P.
中科院分区：
文献类型：
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作者：
Mahajan, Kiran;Mahajan, Nupam P.
AKT/PKB serine threonine kinase, a critical signaling molecule promoting cell growth and survival pathways, is frequently dysregulated in many cancers. Although phosphatidylinositol-3-OH kinase (PI3K), a lipid kinase, is well characterized as a major regulator of AKT activation in response to a variety of ligands, recent studies highlight a diverse group of tyrosine (Ack1/TNK2, Src, PTK6) and serine/threonine (TBK1, IKBKE, DNAPKcs) kinases that activate AKT directly to promote its pro-proliferative signaling functions. While some of these alternate AKT activating kinases respond to growth factors, others respond to inflammatory and genotoxic stimuli. A common theme emerging from these studies is that aberrant or hyperactivation of these alternate kinases is often associated with malignancy. Consequently, evaluating the use of small molecular inhibitors against these alternate AKT activating kinases at earlier stages of cancer therapy may overcome the pressing problem of drug resistance surfacing especially in patients treated with PI3K inhibitors.
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