ArticleOncotarget2015
Depletion of the cisplatin targeted HMGB-box factor UBF selectively induces p53-independent apoptotic death in transformed cells.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 43 citations in OpenAlex.
- Ribosome biogenesis: A central player in liver diseases.Genes & diseases · 2025Review
- APE1 condensation in nucleoli of non-cancer cells depends on rRNA transcription and forming G-quadruplex RNA structures.Nucleic acids research · 2025Article
- Predicting patient outcomes with gene-expression biomarkers from colorectal cancer organoids and cell lines.Frontiers in molecular biosciences · 2025Article
- Honey Targets Ribosome Biogenesis Components to Suppress the Growth of Human Pancreatic Cancer Cells.Cancers · 2024Article
- Polymerase I as a Target for Treating Neurodegenerative Disorders.Biomedicines · 2024Review
- Early maturation and hyperexcitability is a shared phenotype of cortical neurons derived from different ASD-associated mutations.Translational psychiatry · 2023Article
- HMG-boxes, ribosomopathies and neurodegenerative disease.Frontiers in genetics · 2023Review
- Regulation of RNA Polymerase I Stability and Function.Cancers · 2022Review
- Behavioral and molecular effects of Ubtf knockout and knockdown in mice.Brain research · 2022Article
- Review
- UBTF facilitates melanoma progression via modulating MEK1/2-ERK1/2 signalling pathways by promoting GIT1 transcription.Cancer cell international · 2021Article
- Article
- Ribosomal proteins and human diseases: molecular mechanisms and targeted therapy.Signal transduction and targeted therapy · 2021Review
- Review
- The Role ofInternational journal of molecular sciences · 2021Review
- Article
- Review
- Conditional depletion of the RNA polymerase I subunit PAF53 reveals that it is essential for mitosis and enables identification of functional domains.The Journal of biological chemistry · 2019Article
- The Short N-Terminal Repeats of Transcription Termination Factor 1 Contain Semi-Redundant Nucleolar Localization Signals and P19-ARF Tumor Suppressor Binding Sites.The Yale journal of biology and medicine · 2019Article
- HMGB proteins involved in TOR signaling as general regulators of cell growth by controlling ribosome biogenesis.Current genetics · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Cisplatin-DNA adducts act as strong decoys for the Upstream Binding Factor UBF (UBTF) and have been shown to inhibit transcription of the ribosomal RNA genes by RNA polymerase I. However, it is unclear if this plays a significant role in the chemotherapeutic activity of cis- or carboplatin. We find that cisplatin in fact induces a very rapid displacement of UBF from the ribosomal RNA genes and strong inhibition of ribosomal RNA synthesis, consistent with this being an important factor in its cytotoxicity. Using conditional gene deletion, we recently showed that UBF is an essential factor for transcription of the ribosomal RNA genes and for ribosome biogenesis. We now show that loss of UBF arrests cell proliferation and induces fully penetrant, rapid and synchronous apoptosis, as well as nuclear disruption and cell death, specifically in cells subjected to oncogenic stress. Apoptosis is not affected by homozygous deletion of the p53 gene and occurs equally in cells transformed by SV40 T antigens, by Myc or by a combination of Ras & Myc oncogenes. The data strongly argue that inhibition of UBF function is a major factor in the cytotoxicity of cisplatin. Hence, drug targeting of UBF may be a preferable approach to the use of the highly toxic platins in cancer therapy.
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.