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SURF2 is a MDM2 antagonist in triggering the nucleolar stress response
Open accessPreprint — published as 10.1038/s41467-024-52659-x · Paper page
Abstract
Cancer cells are addicted to strong ribosome production to sustain their proliferation rate. Many chemotherapies impede ribosome production which is perceived by cells as “nucleolar stress” (NS), triggering p53-dependent and independent response pathways leading to cell cycle arrest and/or apoptosis. The 5S RNP particle, a sub-ribosomal particle, is instrumental to NS response. Upon ribosome assembly defects, the 5S RNP accumulate as free form. This free form is able to sequester and inhibit MDM2, thus promoting p53 stabilization. To investigate how cancer cells can resist to NS, we purified free-5S RNP and uncovered a new interaction partner, SURF2. Functional characterization of SURF2 shows that its depletion increases cellular sensitivity to NS, while its overexpression promotes their resistance to it. Consistently, SURF2 expression level negatively correlates with the overall survival in adrenocortical and head and neck squamous cell carcinomas. Our data demonstrate that SURF2 buffers free-5S RNP particles, and can modulate their activity. SURF2 regulates NS responses, and is a key player in both ribosomopathies and oncogenic mechanisms.
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Metadata
- Authors
- Tagnères, S., Santo, P. E., Radermecker, J., Rinaldi, D., Froment, C., Provost, Q., Capeille, S., Watkins, N., Marcoux, J., Gleizes, P.-E., Marcel, V., Plisson-Chastang, C., & Lebaron, S.
- Affiliations
- Centre National de la Recherche Scientifique (FR)
- Lyon 1 Université (FR)
- Newcastle University (GB)
- Corresponding author
- Lebaron, Simon
- ORCID
- Venue
- Nature Communications
- Publisher
- openRxiv
- Published
- 2024-01-09
- Volume
- 15
- Issue
- 1
- Pages
- 8404-8404
- ISSN
- 2041-1723 (ISSN-L)
- PMC
- PMC11436901
- OpenAlex
- W4402903566
- Cited by
- 15
- References
- 1
- Citations by year
- 2026: 6 · 2025: 9
- FWCI
- 2.57
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by-nc-nd
- Locations
- Nature Communications (publishedVersion, cc-by-nc-nd)
- bioRxiv (Cold Spring Harbor Laboratory) (acceptedVersion, other-oa)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- HAL (submittedVersion, cc-by-nc-nd)
- RePEc: Research Papers in Economics (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Agence Nationale de la Recherche (ANR-10-INBS-08, ANR-10)
- Institut National de la Santé et de la Recherche Médicale
- Ligue Contre le Cancer (62339)
- Centre National de la Recherche Scientifique
- Institut National Du Cancer (PLBIO022-065)
- Institute of Cancer Research
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nuclear Structure and Function
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › RNA and protein synthesis mechanisms
- Keywords
- nucleolar stress response, ribosome biogenesis, p53 stabilization, tumor resistance, adrenocortical carcinoma, prognostic factors, chemoresistance
- MeSH terms
- RNA-Seq, Antineoplastic Agents, Cell Nucleolus, Cell Survival, Humans, Neoplasms, Proteins, Ribonucleoproteins, Ribosomes, Stress, Physiological, Gene Expression Regulation, Neoplastic, Tumor Suppressor Protein p53, Apoptosis, Cell Line, Tumor, Cell Proliferation, Proto-Oncogene Proteins c-mdm2, Protein Stability
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