mTOR kinase leads to PTEN-loss-induced cellular senescence by phosphorylating p53

Jung, Seung Hee; Hwang, Hyun Jung; Kang, Donghee; Park, Hyun A.; Lee, Hyung Chul; Jeong, Daecheol; Lee, Keunwook; Park, Heon Joo; Ko, Young-Gyu; Lee, Jae-Seon

doi:10.1038/s41388-018-0521-8

Cited by 167PI3K/AKT/mTOR signaling in cancerTelomeres, Telomerase, and SenescenceCancer-related Molecular Pathways

mTOR kinase leads to PTEN-loss-induced cellular senescence by phosphorylating p53

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Jung, Seung Hee, Hwang, Hyun Jung, Kang, Donghee, Park, Hyun A., Lee, Hyung Chul, Jeong, Daecheol, Lee, Keunwook, Park, Heon Joo +2 more·2019·Oncogene

DOI 10.1038/s41388-018-0521-8PMC PMC6755978

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Abstract

Loss of PTEN, the major negative regulator of the PI3K/AKT pathway induces a cellular senescence as a failsafe mechanism to defend against tumorigenesis, which is called PTEN-loss-induced cellular senescence (PICS). Although many studies have indicated that the mTOR pathway plays a critical role in cellular senescence, the exact functions of mTORC1 and mTORC2 in PICS are not well understood. In this study, we show that mTOR acts as a critical relay molecule downstream of PI3K/AKT and upstream of p53 in PICS. We found that PTEN depletion induces cellular senescence via p53-p21 signaling without triggering DNA damage response. mTOR kinase, a major component of mTORC1 and mTORC2, directly binds p53 and phosphorylates it at serine 15. mTORC1 and mTORC2 compete with MDM2 and increase the stability of p53 to induce cellular senescence via accumulation of the cell cycle inhibitor, p21. In embryonic fibroblasts of PTEN-knockout mice, PTEN deficiency also induces mTORC1 and mTORC2 to bind to p53 instead of MDM2, leading to cellular senescence. These results collectively demonstrate for the first time that mTOR plays a critical role in switching cells from proliferation signaling to senescence signaling via a direct link between the growth-promoting activity of AKT and the growth-suppressing activity of p53.

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In PTEN-loss in vitro models of induced senescence, activated mTOR kinase in mTORC1 or mTORC2 stabilizes p53 and triggers the senescent state.
“In PTEN - loss invitro models of induced senescence, the activated mTOR kinase in mTORC1 or mTORC2 stabilizes p53 and triggers the senescent state 39 .”
From Senescence and cancer — role and therapeutic opportunities (2022) · cites this paper as [39]

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mTOR directly phosphorylates p53 in PTEN-loss-induced cellular senescence
Hwang, H. J., Jung, S. H., Kang, D., Park, H. A., Lee, H. C., Jeong, D., Lee, K., & Park, H. J. (2018)
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ORIGINAL ARTICLE
(2016)
DNA damaging agents and p53 do not cause senescence in quiescent cells, while consecutive re-activation of mTOR is associated with conversion to senescence
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The choice between p53-induced senescence and quiescence is determined in part by the mTOR pathway.
Korotchkina, L. G., Leontieva, O. V., Bukreeva, E. I., Demidenko, Z. N., Gudkov, A. V., & Blagosklonny, M. V. (2010) · Aging · doi:10.18632/aging.100160 · Cited by 278 · see citing works

Authors: Jung, S. H., Hwang, H. J., Kang, D., Park, H. A., Lee, H. C., Jeong, D., Lee, K., Park, H. J., Ko, Y.-G., & Lee, J.-S.
Affiliations: Inha University (KR)
Hallym University (KR)
Korea University (KR)
Corresponding author: Lee, Jae-Seon
ORCID: Jung, Seung Hee
Hwang, Hyun Jung
Jeong, Daecheol
Park, Heon Joo
Lee, Jae-Seon
Venue: Oncogene
Publisher: Springer Science and Business Media LLC
Published: 2018-10-18
Volume: 38
Issue: 10
Pages: 1639-1650
ISSN: 0950-9232 (ISSN-L)
1476-5594
DOI: 10.1038/s41388-018-0521-8
PMC: PMC6755978
OpenAlex: W2897025166
Cited by: 166
References: 39
Citations by year: 2026: 15 · 2025: 18 · 2024: 36 · 2023: 20 · 2022: 28 · 2021: 21 · 2020: 19 · 2019: 9
FWCI: 4.36
Type: journal article
Language: en
Open access: hybrid
doi.org
Licence: cc-by
creativecommons.org/licenses/by/4.0 (tdm)
Locations: Oncogene (publishedVersion, cc-by)
PubMed Central (publishedVersion, cc-by)
PubMed (publishedVersion)
Funders: National Research Foundation (2014R1A5A2009392)
Ministry of Science and ICT, South Korea
University of Illinois at Urbana-Champaign
Medical Research Council
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
Keywords: mTOR, PTEN loss, cellular senescence, p53 phosphorylation, p21, MDM2, mTORC1, mTORC2, PI3K/Akt signaling, p53 stabilization, Pten knockout mice, embryonic fibroblasts, tumor suppression
MeSH terms: Mechanistic Target of Rapamycin Complex 1, Mechanistic Target of Rapamycin Complex 2, Animals, Fibroblasts, Humans, Phosphorylation, Signal Transduction, Tumor Suppressor Protein p53, Cellular Senescence, Cell Proliferation, PTEN Phosphohydrolase, Mice, TOR Serine-Threonine Kinases, MCF-7 Cells

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mTOR kinase leads to PTEN-loss-induced cellular senescence by phosphorylating p53

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