ArticleOncotarget2017
The ribosomal protein gene RPL5 is a haploinsufficient tumor suppressor in multiple cancer types.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
96 citing papers in PubMed, 121 citations in OpenAlex.
- Prognostic Value of EEF1A1 and Its Correlation with Immune Regulation in Kidney Renal Clear Cell Carcinoma.Cancers · 2026Article
- The Nucleolus in Human Disease: Ribosome Biogenesis, Nucleolar Surveillance, and Therapeutic Opportunities.Biomolecules · 2026Review
- Histopathological evaluation of RPL5 expression in triple-negative breast cancer: an integrated immunohistochemical and transcriptomic study.European journal of histochemistry : EJH · 2026Article
- RiboScreenBiomedicines · 2026Review
- Article
- Article
- Mutant ribosomal protein RPS15 drives B cell malignancy through oxidative stress and genomic instability.Nature communications · 2026Article
- Complex landscape of somatic copy number alterations in head and neck paragangliomas.Frontiers in endocrinology · 2026Article
- RPL5 deficiency-induced ribosomal stress targets a select subset of proteins and inhibits the PI3K-Akt-mTOR signaling pathway to eradicate leukemia stem cells.Cell death & disease · 2025Article
- Integrated Bioinformatics Analysis of Differentially Expressed RNA-Binding Proteins in Human Gliomas.Cellular and molecular neurobiology · 2025Article
- Significance of the association between hypoxia and pyroptosis-related genes in the prognostic prediction of glioblastoma: insights from model construction and validation.Translational cancer research · 2025Article
- Extra-Ribosomal Roles for Ribosomal Proteins and Their Relevance to Tumour Suppression, Carcinogenesis and Cancer Progression.Cancers · 2025Review
- Elucidating the Role ofCurrent issues in molecular biology · 2025Review
- Review
- Ribosomal protein L5 induces cellular senescence via p53-p21-pRb pathway to mediate relapse of acute myeloid leukemia.Scientific reports · 2025Article
- 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
- Differential impacts of ribosomal protein haploinsufficiency on mitochondrial function.The Journal of cell biology · 2025Article
- Ribosome biogenesis rate, a parameter of sensitivity to chemotherapeutic drugs inhibiting rRNA synthesis.Oncology reviews · 2025Review
- Article
36 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
For many years, defects in the ribosome have been associated to cancer. Recently, somatic mutations and deletions affecting ribosomal protein genes were identified in a few leukemias and solid tumor types. However, systematic analysis of all 81 known ribosomal protein genes across cancer types is lacking. We screened mutation and copy number data of respectively 4926 and 7322 samples from 16 cancer types and identified six altered genes (RPL5, RPL11, RPL23A, RPS5, RPS20 and RPSA). RPL5 was located at a significant peak of heterozygous deletion or mutated in 11% of glioblastoma, 28% of melanoma and 34% of breast cancer samples. Moreover, patients with low RPL5 expression displayed worse overall survival in glioblastoma and in one breast cancer cohort. RPL5 knockdown in breast cancer cell lines enhanced G2/M cell cycle progression and accelerated tumor progression in a xenograft mouse model. Interestingly, our data suggest that the tumor suppressor role of RPL5 is not only mediated by its known function as TP53 or c-MYC regulator. In conclusion, RPL5 heterozygous inactivation occurs at high incidence (11-34%) in multiple tumor types, currently representing the most common somatic ribosomal protein defect in cancer, and we demonstrate a tumor suppressor role for RPL5 in breast cancer.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.