ArticleOncotarget2017
Cancer-mutated ribosome protein L22 (RPL22/eL22) suppresses cancer cell survival by blocking p53-MDM2 circuit.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 64 citations in OpenAlex.
- The Nucleolus in Human Disease: Ribosome Biogenesis, Nucleolar Surveillance, and Therapeutic Opportunities.Biomolecules · 2026Review
- FBXO5 regulates RPL23A to promote MDM2-mediated p53 degradation and facilitate malignant progression of breast cancer.Breast cancer research : BCR · 2026Article
- Fatal Disease Progression Driven by Acquired MET Amplification After EGFR-TKI Therapy in EGFR- and RBM10-Mutant Lung Adenocarcinoma.Cancer management and research · 2026Article
- Article
- Extra-Ribosomal Roles for Ribosomal Proteins and Their Relevance to Tumour Suppression, Carcinogenesis and Cancer Progression.Cancers · 2025Review
- Article
- Ribosome specialization by cancer-associated ribosomal protein mutations: progress made and open questions.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025Review
- Ribosome biogenesis rate, a parameter of sensitivity to chemotherapeutic drugs inhibiting rRNA synthesis.Oncology reviews · 2025Review
- RPL22 is a tumor suppressor in MSI-high cancers and a splicing regulator of MDM4.Cell reports · 2024Article
- Article
- Ribosome profiling: a powerful tool in oncological research.Biomarker research · 2024Review
- Decoding Ribosome Heterogeneity: A New Horizon in Cancer Therapy.Biomedicines · 2024Review
- Ribosome subunit attrition and activation of the p53-MDM4 axis dominate the response of MLL-rearranged cancer cells to WDR5 WIN site inhibition.bioRxiv : the preprint server for biology · 2024Article
- RPL22 is a tumor suppressor in MSI-high cancers and a key splicing regulator of MDM4.bioRxiv : the preprint server for biology · 2023Article
- RNA-binding motif protein 10 inactivates c-Myc by partnering with ribosomal proteins uL18 and uL5.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Convergent somatic evolution commences in utero in a germline ribosomopathy.Nature communications · 2023Article
- Ribosomal Profiling by Gradient Fractionation of Cell Lysates.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Deficiency of ribosomal proteins reshapes the transcriptional and translational landscape in human cells.Nucleic acids research · 2022Article
- Ribosome heterogeneity in Drosophila melanogaster gonads through paralog-switching.Nucleic acids research · 2022Article
- Loss of RPS27a expression regulates the cell cycle, apoptosis, and proliferation via the RPL11-MDM2-p53 pathway in lung adenocarcinoma cells.Journal of experimental & clinical cancer research : CR · 2022Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
Several ribosomal proteins (RPs) in response to various ribosomal stressors have been shown to play a critical role in p53-dependent regulation of cell cycle arrest, apoptosis and tumor suppression. Here, we report ribosomal protein L22 (RPL22/eL22) as a novel p53 activator highly mutated (mostly deletion mutation) in various types of human cancers, but not essential for ribosomal biogenesis in normal cells. Ectopic expression of RPL22/eL22 suppressed the colony formation of cancer cells in a p53-dependent manner, whereas knockdown of RPL22/eL22 significantly compromised p53 activation by Actinomycin D, rescuing p53-induced G1/G0 cell cycle arrest. Interestingly, human tumors with RPL22/eL22 deletion appeared to sustain wild type p53. Mechanistically, RPL22/eL22 bound to MDM2 acidic domain and inhibited MDM2-mediated p53 ubiquitination and degradation, hence extending the half-life of p53. Ribosome-profiling analysis revealed that induction of ribosomal stress by Actinomycin D leads to the increase of ribosome-free RPL22/eL22 pool. Also, RPL22/eL22 formed a complex with MDM2/RPL5/uL18/RPL11/uL5 and synergized with RPL11/uL5 to activate p53. Furthermore, the N terminus of RPL22/eL22 bound to MDM2, while the C terminus interacted with RPL5/uL18/RPL11/uL5; both of these two fragments activated p53 by inhibiting MDM2. Our study indicates that RPL22/eL22 highly mutated in human cancers plays an anti-cancer role likely through regulation of the MDM2-p53 feedback loop, and also suggests that targeting the RPL22/eL22-MDM2-p53 pathway could be a potential strategy for future development of anti-cancer therapy.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.