The Akt-mTOR tango and its relevance to cancer.

By N. Hay. Cancer Cell, 2005

819 citations recorded by the source corpus.

Subfields: Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/455705cacec0b2f518f866f9b18a21389b6a65d7

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Citations in the corpus

Akt determines replicative senescence and oxidative or oncogenic premature senescence and sensitizes cells to oxidative apoptosis (2008, background): “Most importantly, we showed that rapamycin, which is usually cytostatic, sensitizes cells to ROS-mediated cell death because it also activates Akt via the inhibition of a negative feedback loop (Bhaskar and Hay, 2007; Harrington et al., 2005; Hay, 2005).”
Pten regulates neuronal arborization and social interaction in mice. (2006, neutral): “NF1, PTEN, and the TSC complex are negative regulators of the PI3K pathway, and inactivation of any of the proteins results in a hyperactive signal transduction in many circumstances (Hay, 2005; Klesse and Parada, 1998; Manning and Cantley, 2003).”
FoxOs are lineage-restricted redundant tumor suppressors and regulate endothelial cell homeostasis. (2007, neutral): “Recently, much attention has been focused on TSC2 and mTOR signaling as mounting pharmacological evidence suggests that mTOR is the prime effector of the PI3K-AKT pathway, with TSC2 serving as a central node linking LKB1-AMPK and PI3K-AKT with mTOR (Hay, 2005).”
SIN1/MIP1 maintains rictor-mTOR complex integrity and regulates Akt phosphorylation and substrate specificity. (2006, background): “Thus the mTOR pathway is an attractive anticancer drug target (Guertin and Sabatini, 2005; Hay, 2005).”
Akt-dependent regulation of NF-{kappa}B is controlled by mTOR and Raptor in association with IKK. (2008, background): “For example, Akt phosphorylates and inactivates Foxo proteins that are proapoptotic through their ability to regulate the expression of genes that encode proteins that promote cell death (Tran et al. 2003; see Hay 2005).”
Pulmonary neuroendocrine (carcinoid) tumors: European Neuroendocrine Tumor Society expert consensus and recommendations for best practice for typical and atypical pulmonary carcinoids. (2015, background): “Mammalian target of Rapamycin (mtor) has been identified as a kinase activated in the PI3K signaling pathway of lung NETs [165].”
Rapamycin induces feedback activation of Akt signaling through an IGF-1R-dependent mechanism (2007, background): “Hyperactivation of Akt is associated with resistance to apoptosis, increased cell growth, cell proliferation and cell energy metabolism (Hay, 2005).”
Targeting PI3K/Akt signal transduction for cancer therapy (2021, background): “This step is limited by a negative regulator of mTOR named PTEN.(81) Akt and mTOR are thought to interact, as Akt was shown to activate mTOR through the phosphorylation of tuberous sclerosis complex 2 (TSC2).”
Current development of mTOR inhibitors as anticancer agents (2006, background): “Mammalian target of rapamycin ( mTOR , also known as FRAP, RAFT1 and RAP1) has been identified as a key kinase acting downstream of the activation of PI3”
Ras, PI(3)K and mTOR signalling controls tumour cell growth (2006, background): “and perhaps competition between the rictor-mediated and raptor-mediated assembly of mTOR complexe”
Exploiting the PI3K/AKT Pathway for Cancer Drug Discovery (2005, background): “Indeed, mTOR inhibition by rapamycin or rapamycin analogues can activate upstream proteins including AKT, which is probably a result of loss of feedback inhibitio”
A dual PI3 kinase/mTOR inhibitor reveals emergent efficacy in glioma. (2006, neutral): “It has recently been proposed that selective mTOR inhibition may lead to PI3 kinase activation, thereby limiting the effectiveness of these agents (Hay, 2005).”