ArticleProceedings of the National Academy of Sciences of the United States of America2001
A role of the kinase mTOR in cellular transformation induced by the oncoproteins P3k and Akt.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 122 papers.
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Who cites it
122 citing papers in PubMed, 292 citations in OpenAlex.
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- Fundamental Clock of Biological Aging: Convergence of Molecular, Neurodegenerative, Cognitive and Psychiatric Pathways: Non-Equilibrium Thermodynamics Meet Psychology.International journal of molecular sciences · 2021Review
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- Autophagy Inhibition Potentiates the Anticancer Effects of a Bendamustine Derivative NL-101 in Acute T Lymphocytic Leukemia.BioMed research international · 2020Article
- Molecular Determinants of Cancer Therapy Resistance to HDAC Inhibitor-Induced Autophagy.Cancers · 2019Review
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- Targeting the BDNF/TrkB pathway for the treatment of tumors.Oncology letters · 2019Review
- Repeated Systemic Treatment with Rapamycin Affects Behavior and Amygdala Protein Expression in Rats.The international journal of neuropsychopharmacology · 2018Article
- EGFR and AKT1 overexpression are mutually exclusive and associated with a poor survival in resected gastric adenocarcinomas.Cancer biomarkers : section A of Disease markers · 2018Article
- Vernodalol mediates antitumor effects in acute promyelocytic leukemia cells.Oncology letters · 2018Article
- Novel Factors of Viral Origin Inhibit TOR Pathway Gene Expression.Frontiers in physiology · 2018Article
- Pilot study of sirolimus in patients with PIK3CA mutant/amplified refractory solid cancer.Molecular and clinical oncology · 2017Article
- Sestrin-3 modulation is essential for therapeutic efficacy of cucurbitacin B in lung cancer cells.Carcinogenesis · 2017Article
- NADPH oxidase promotes Parkinsonian phenotypes by impairing autophagic flux in an mTORC1-independent fashion in a cellular model of Parkinson's disease.Scientific reports · 2016Article
62 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The oncoproteins P3k (homolog of the catalytic subunit of class IA phosphoinositide 3-kinase) and Akt (protein kinase B) induce oncogenic transformation of chicken embryo fibroblasts. The transformed cells show constitutive phosphorylation of the positive regulator of translation p70S6 kinase (S6K) and of the eukaryotic initiation factor 4E-BP1 binding protein (4E-BP1), a negative regulator of translation. Phosphorylation activates S6K and inactivates 4E-BP1. A mutant of Akt that retains kinase activity but does not induce phosphorylation of S6K or of 4E-BP1 fails to transform chicken embryo fibroblasts, suggesting a correlation between the oncogenicity of Akt and phosphorylation of S6K and 4E-BP1. The macrolide antibiotic rapamycin effectively blocks oncogenic transformation induced by either P3k or Akt but does not reduce the transforming activity of 11 other oncoproteins. Rapamycin inhibits the kinase mTOR, an important regulator of translation, and this inhibition requires binding of the antibiotic to the immunophilin FKBP12. Displacement of rapamycin from FKBP12 relieves the inhibition of mTOR and also restores P3k-induced transformation. These data are in accord with the hypothesis that transformation by P3k or Akt involves intervention in translational controls.
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