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Ref Type Journal Article
PMID (25551293)
Authors Vivanco I, Chen ZC, Tanos B, Oldrini B, Hsieh WY, Yannuzzi N, Campos C, Mellinghoff IK
Title A kinase-independent function of AKT promotes cancer cell survival.
Journal eLife
Vol 3
Date 2014
Abstract Text The serine-threonine kinase AKT regulates proliferation and survival by phosphorylating a network of protein substrates. In this study, we describe a kinase-independent function of AKT. In cancer cells harboring gain-of-function alterations in MET, HER2, or Phosphatidyl-Inositol-3-Kinase (PI3K), catalytically inactive AKT (K179M) protected from drug induced cell death in a PH-domain dependent manner. An AKT kinase domain mutant found in human melanoma (G161V) lacked enzymatic activity in vitro and in AKT1/AKT2 double knockout cells, but promoted growth factor independent survival of primary human melanocytes. ATP-competitive AKT inhibitors failed to block the kinase-independent function of AKT, a liability that limits their effectiveness compared to allosteric AKT inhibitors. Our results broaden the current view of AKT function and have important implications for the development of AKT inhibitors for cancer.


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Molecular Profile Treatment Approach
Gene Name Source Synonyms Protein Domains Gene Description Gene Role
Therapy Name Drugs Efficacy Evidence Clinical Trials
Drug Name Trade Name Synonyms Drug Classes Drug Description
Gene Variant Impact Protein Effect Variant Description Associated with drug Resistance
AKT1 G311D missense unknown AKT1 G311D lies within the protein kinase domain of the Akt1 protein ( The functional effect of G311D is conflicting as it results in decreased kinase activity, demonstrated by impaired phosphorylation of Akt substrates in cell culture in one study (PMID: 25551293), but results in reduced Akt hydroxylation, increased Akt phosphorylation at T308, and increased colony formation in cell culture in another study (PMID: 27563096).
Molecular Profile Indication/Tumor Type Response Type Therapy Name Approval Status Evidence Type Efficacy Evidence References
AKT1 W80A breast cancer resistant MK2206 Preclinical Actionable In a preclinical study, breast cancer cells expressing AKT1 W80A were resistant to MK2206 in culture, resulting in repression of induced cell death when compared to wild-type AKT1 (PMID: 25551293). 25551293