Tumor suppressor activity of the ERK/MAPK pathway by promoting selective protein degradation
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Constitutive activation of growth factor signaling pathways paradoxically triggers a cell cycle arrest known as cellular senescence. In primary cells expressing oncogenic ras, this mechanism effectively prevents cell transformation. Surprisingly, attenuation of ERK/MAP kinase signaling by genetic inactivation of Erk2, RNAi-mediated knockdown of ERK1 or ERK2, or MEK inhibitors prevented the activation of the senescence mechanism, allowing oncogenic ras to transform primary cells. Mechanistically, ERK-mediated senescence involved the proteasome-dependent degradation of proteins required for cell cycle progression, mitochondrial functions, cell migration, RNA metabolism, and cell signaling. This senescence-associated protein degradation (SAPD) was observed not only in cells expressing ectopic ras , but also in cells that senesced due to short telomeres. Individual RNAi-mediated inactivation of SAPD targets was sufficient to restore senescence in cells transformed by oncogenic ras or trigger senescence in normal cells. Conversely, the anti-senescence viral oncoproteins E1A, E6, and E7 prevented SAPD. In human prostate neoplasms, high levels of phosphorylated ERK were found in benign lesions, correlating with other senescence markers and low levels of STAT3, one of the SAPD targets. We thus identified a mechanism that links aberrant activation of growth signaling pathways and short telomeres to protein degradation and cellular senescence.
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Aberrant Ras/ERK signaling leads to senescence-associated protein degradation (SAPD), whose targets include proteins required for cell cycle progression, cell migration, mitochondrial functions, RNA metabolism, and cell signaling.
“It was recently shown that aberrant Ras/ERK signaling leads to senescence-associated protein degradation (SAPD), whose targets include proteins required for cell cycle progression, cell migration, mitochondrial functions, RNA metabolism, and cell signaling (Deschênes-Simard et al. 2013).”
From Cellular senescence and its effector programs (2014) · cites this paper as Deschênes-Simard et al. 2013
Inactivation of individual SAPD targets is sufficient for senescence induction.
“Inactivation of individual SAPD targets is sufficient for senescence induction.”
From Cellular senescence and its effector programs (2014) · cites this paper as Deschênes-Simard et al. 2013
PML and ERK were found in benign human prostatic hyperplasia-derived samples.
“PML and ERK were found in benign human prostatic hyperplasia- derived samples 85,86 .”
From Senescence and cancer — role and therapeutic opportunities (2022) · cites this paper as [86]
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- Authors
- Deschênes-Simard, X., Gaumont-Leclerc, M.-F., Bourdeau, V., Lessard, F., Moiseeva, O., Forest, V., Igelmann, S., Mallette, F. A., Saba-El-Leil, M. K., Meloche, S., Saad, F., Mes-Masson, A.-M., & Ferbeyre, G.
- Affiliations
- Université de Montréal (CA)
- Centre Hospitalier de l’Université de Montréal (CA)
- Institute for Research in Immunology and Cancer (CA)
- ORCID
- Venue
- Genes & Development
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2013-04-15
- Volume
- 27
- Issue
- 8
- Pages
- 900-915
- ISSN
- 0890-9369 (ISSN-L)
- 1549-5477
- PMC
- PMC3650227
- OpenAlex
- W1978818809
- Cited by
- 194
- References
- 60
- Citations by year
- 2026: 4 · 2025: 14 · 2024: 7 · 2023: 19 · 2022: 16 · 2021: 19 · 2020: 18 · 2019: 19 · 2018: 19 · 2017: 14 · 2016: 13 · 2015: 9 · 2014: 16 · 2013: 7
- Type
- posted content
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Genes & Development (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Canadian Institutes of Health Research
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Melanoma and MAPK Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- cellular senescence, ERK signaling, oncogenic Ras, protein degradation, short telomeres, tumor suppressor activity, MEK inhibitors, STAT3, viral oncoproteins, prostate cancer, proteasome
- MeSH terms
- Animals, Cell Line, Cell Transformation, Neoplastic, Female, Fibroblasts, Humans, Male, Mice, Inbred BALB C, Prostatic Neoplasms, Cellular Senescence, Mice, Knockout, ras Proteins, MAP Kinase Signaling System, Tumor Suppressor Proteins, Proteasome Endopeptidase Complex, Mice, Gene Knockdown Techniques, Proteolysis
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