ArticleOncotarget2015
The 5'-untranslated region of p16INK4a melanoma tumor suppressor acts as a cellular IRES, controlling mRNA translation under hypoxia through YBX1 binding.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- Current Practice in Bicistronic IRES Reporter Use: A Systematic Review.International journal of molecular sciences · 2021Pooled it
- Integrating rna structure and protein interactions to uncover the mechanisms of viral and cellular ires function.Biology direct · 2025Article
- Exploring p53 isoforms: unraveling heterogeneous p53 tumor suppressor functionality in uveal melanoma.Cell death discovery · 2025Article
- Internal ribosome entry sites enhance translation in trans in antisense non-coding SINEUP and circular RNAs.Nucleic acids research · 2025Article
- YBX1: an RNA/DNA-binding protein that affects disease progression.Frontiers in oncology · 2025Review
- YBX1: A Multifunctional Protein in Senescence and Immune Regulation.Current issues in molecular biology · 2024Review
- The Abl1 tyrosine kinase is a key player in doxorubicin-induced cardiomyopathy and its p53/p73 cell death mediated signaling differs in atrial and ventricular cardiomyocytes.Journal of translational medicine · 2024Article
- Y-Box Binding Protein 1: Unraveling the Multifaceted Role in Cancer Development and Therapeutic Potential.International journal of molecular sciences · 2024Review
- Biomarkers of aging.Science China. Life sciences · 2023Review
- ETV7 reduces inflammatory responses in breast cancer cells by repressing the TNFR1/NF-κB axis.Cell death & disease · 2023Article
- Article
- IRES Trans-Acting Factors, Key Actors of the Stress Response.International journal of molecular sciences · 2019Review
- DAP5 increases axonal outgrowth of hippocampal neurons by enhancing the cap-independent translation of DSCR1.4 mRNA.Cell death & disease · 2019Article
- More than just scanning: the importance of cap-independent mRNA translation initiation for cellular stress response and cancer.Cellular and molecular life sciences : CMLS · 2017Review
- Functional analysis of a CDKN2A 5'UTR germline variant associated with pancreatic cancer development.PloS one · 2017Article
- IRES-dependent translation of the long non coding RNA meloe in melanoma cells produces the most immunogenic MELOE antigens.Oncotarget · 2016Article
- Cap-Independent Translational Control of Carcinogenesis.Frontiers in oncology · 2016Review
- A Novel Method for Gene-Specific Enhancement of Protein Translation by Targeting 5'UTRs of Selected Tumor Suppressors.PloS one · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 6 institutions in 4 countries.
Funding
Abstract
CDKN2A/p16INK4a is an essential tumor suppressor gene that controls cell cycle progression and replicative senescence. It is also the main melanoma susceptibility gene. Here we report that p16INK4a 5'UTR mRNA acts as a cellular Internal Ribosome Entry Site (IRES). The potential for p16INK4a 5'UTR to drive cap-independent translation was evaluated by dual-luciferase assays using bicistronic and monocistronic vectors. Results of reporters' relative activities coupled to control analyses for actual bicistronic mRNA transcription, indicated that the wild type p16INK4a 5'UTR could stimulate cap-independent translation. Notably, hypoxic stress and the treatment with mTOR inhibitors enhanced the translation-stimulating property of p16INK4a 5'UTR. RNA immunoprecipitation performed in melanoma-derived SK-Mel-28 and in a patient-derived lymphoblastoid cell line indicated that YBX1 can bind the wild type p16INK4a mRNA increasing its translation efficiency, particularly during hypoxic stress. Modulation of YBX1 expression further supported its involvement in cap-independent translation of the wild type p16INK4a but not a c.-42T>A variant. RNA SHAPE assays revealed local flexibility changes for the c.-42T>A variant at the predicted YBX1 binding site region. Our results indicate that p16INK4a 5'UTR contains a cellular IRES that can enhance mRNA translation efficiency, in part through YBX1.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.