ArticlePloS one2010
Silencing of ribosomal protein S9 elicits a multitude of cellular responses inhibiting the growth of cancer cells subsequent to p53 activation.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 82 citations in OpenAlex.
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- Identification of Key Prognostic Alternative Splicing Events of Costimulatory Molecule-Related Genes in Colon Cancer.Combinatorial chemistry & high throughput screening · 2024Article
- The dark side of mRNA translation and the translation machinery in glioblastoma.Frontiers in cell and developmental biology · 2023Review
- Unravelling the neuroprotective mechanisms of carotenes in differentiated human neural cells: Biochemical and proteomic approaches.Food chemistry. Molecular sciences · 2022Article
- 6-Hydroxydopamine Induces Neurodegeneration in Terminally Differentiated SH-SY5Y Neuroblastoma Cells via Enrichment of the Nucleosomal Degradation Pathway: a Global Proteomics Approach.Journal of molecular neuroscience : MN · 2022Article
- Article
- RPS9 promotes the progression of NSCLC via activation Stat3 and Erk signaling pathways.Journal of Cancer · 2022Article
- Regulatory Networks of Prognostic mRNAs in Pediatric Acute Myeloid Leukemia.Journal of healthcare engineering · 2022Article
- Deficiency of the Ribosomal Protein uL5 Leads to Significant Rearrangements of the Transcriptional and Translational Landscapes in Mammalian Cells.International journal of molecular sciences · 2021Article
- Localization and Functional Roles of Components of the Translation Apparatus in the Eukaryotic Cell Nucleus.Cells · 2021Review
- Ribosomal proteins and human diseases: molecular mechanisms and targeted therapy.Signal transduction and targeted therapy · 2021Review
- Multiomic analysis of Schistosoma mansoni reveals unique expression profiles in cercarial heads and tails.Communications biology · 2021Article
- Article
- Analysis of U8 snoRNA Variants in Zebrafish Reveals How Bi-allelic Variants Cause Leukoencephalopathy with Calcifications and Cysts.American journal of human genetics · 2020Article
- Events of alternative splicing in head and neck cancer via RNA sequencing - an update.BMC genomics · 2019Article
- Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDisruption of the nucleolus often leads to activation of the p53 tumor suppressor pathway through inhibition of MDM2 that is mediated by a limited set of ribosomal proteins including RPL11 and RPL5. The effects of ribosomal protein loss in cultured mammalian cells have not been thoroughly investigated. Here we characterize the cellular stress response caused by depletion of ribosomal protein S9 (RPS9). METHODOLOGY/PRINCIPAL
findingsDepletion of RPS9 impaired production of 18S ribosomal RNA and induced p53 activity. It promoted p53-dependent morphological differentiation of U343MGa Cl2:6 glioma cells as evidenced by intensified expression of glial fibrillary acidic protein and profound changes in cell shape. U2OS osteosarcoma cells displayed a limited senescence response with increased expression of DNA damage response markers, whereas HeLa cervical carcinoma cells underwent cell death by apoptosis. Knockdown of RPL11 impaired p53-dependent phenotypes in the different RPS9 depleted cell cultures. Importantly, knockdown of RPS9 or RPL11 also markedly inhibited cell proliferation through p53-independent mechanisms. RPL11 binding to MDM2 was retained despite decreased levels of RPL11 protein following nucleolar stress. In these settings, RPL11 was critical for maintaining p53 protein stability but was not strictly required for p53 protein synthesis.
conclusionsp53 plays an important role in the initial restriction of cell proliferation that occurs in response to decreased level of RPS9. Our results do not exclude the possibility that other nucleolar stress sensing molecules act upstream or in parallel to RPL11 to activate p53. Inhibiting the expression of certain ribosomal proteins, such as RPS9, could be one efficient way to reinitiate differentiation processes or to induce senescence or apoptosis in rapidly proliferating tumor cells.
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