Activation of Akt and eIF4E survival pathways by rapamycin-mediated mammalian target of rapamycin inhibition.

By Shi-Yong Sun, L. Rosenberg, Xuerong Wang, Zhongmei Zhou, P. Yue, H. Fu, F. Khuri. Cancer Research, 2005

843 citations recorded by the source corpus.

Subfields: Information Systems, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/3a81923dda3ba646ac2d57639bca994ce174f0ae

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Citations in the corpus

A dual PI3 kinase/mTOR inhibitor reveals emergent efficacy in glioma. (2006, neutral): “Although these compounds are cytostatic in many preclinical studies (Easton and Houghton, 2004; Takeuchi et al., 2005), mTOR inhibitors have failed to achieve similar cytostasis in clinical trials (Margolin et al., 2005), suggesting that the utility of these agents may be improved through…”
The PTEN–PI3K pathway: of feedbacks and cross-talks (2008, background): “Another study proposes that eIF4E activation leads to AKT activation through a Nijmegen breakage syndrome 1-PI3K-dependent mechanism (Culjkovic et al., 2008) and conversely, PI3K has been proposed to signal directly to eIF4E upon rapamycin treatment (Sun et al., 2005).”
Rapamycin induces feedback activation of Akt signaling through an IGF-1R-dependent mechanism (2007, result): “Our results are consistent with recent reports that rapamycin induces Akt activation in human nonsmall-cell lung cancer and breast cancer cell lines (Sun et al., 2005; O’Reilly et al., 2006).”
Small molecule inhibition of the autophagy kinase ULK1 and identification of ULK1 substrates (2015, background): “SBI-0206965 Suppresses Autophagy Induced by mTOR Inhibition, and This Is Phenocopied by ULK1 siRNA To test the ability of 6965 to block autophagy and cell survival, initial studies were performed in A549 lung cancer cells, which are highly sensitive to mTOR inhibition (Sun et al., 2005).”
Ras, PI(3)K and mTOR signalling controls tumour cell growth (2006, background): “The existence of the S6K-based negative-feedback loop means that prolonged rapamycin treatment will probably lead to enhanced PI(3)K–AKT activation in some tumours, as has been observed in several tumour cell lines grown in culture, and in tissues from patients in clinical trials of rapamycin analog”
Antitumor Activity of Rapamycin in a Phase I Trial for Patients with Recurrent PTEN-Deficient Glioblastoma (2008, background): “As predicted from preclinical studies [27,28], rapamycin also led to the activation of Akt in some cases, and this activation was significantly correlated with shorter timeto-tumor progression.”
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”
mTOR inhibition induces upstream receptor tyrosine kinase signaling and activates Akt. (2006, background): “As measured by an in vitro kinase assay, Akt activity in DU-145 increased in parallel with the induction of phosphorylation and was elevated 3-fold compared with controls 4 hours after the addition of the drug ( The increase in GSK3a/h phosphorylation occurred in both DU-145 and MCF-7 cells and bega”
Autophagy as a target for anticancer therapy (2011, background): “Akt is also activated via phosphorylation by mTORC2, providing positive feedback that contributes to inhibition of autophagy”