ArticleMolecular and cellular biology2000
Repression of RNA polymerase I transcription by the tumor suppressor p53.
Article in Molecular and cellular biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 151 papers.
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Who cites it
151 citing papers in PubMed, 282 citations in OpenAlex.
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- The G-quadruplex ligand CX-5461: an innovative candidate for disease treatment.Journal of translational medicine · 2025Review
- Genome-wide screening in human embryonic stem cells identifies genes and pathways involved in the p53 pathway.Molecular medicine (Cambridge, Mass.) · 2025Article
- Ribosome biogenesis rate, a parameter of sensitivity to chemotherapeutic drugs inhibiting rRNA synthesis.Oncology reviews · 2025Review
- LINC01116-dependent upregulation of RNA polymerase I transcription drives oncogenic phenotypes in lung adenocarcinoma.Journal of translational medicine · 2024Article
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- POLR1D silencing suppresses lung cancer cells proliferation and migration via inhibition of PI3K-Akt pathway.Journal of cardiothoracic surgery · 2024Article
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- Intra-promoter switch of transcription initiation sites in proliferation signaling-dependent RNA metabolism.Nature structural & molecular biology · 2023Article
- Fallopian tube lesions as potential precursors of early ovarian cancer: a comprehensive proteomic analysis.Cell death & disease · 2023Article
- Targeting RNA Polymerase I Transcription Activity in Osteosarcoma: Pre-Clinical Molecular and Animal Treatment Studies.Biomedicines · 2023Article
- RNA Polymerases I and III in development and disease.Seminars in cell & developmental biology · 2023Review
- Cell cycle control by the insulin-like growth factor signal: at the crossroad between cell growth and mitotic regulation.Cell cycle (Georgetown, Tex.) · 2023Review
- Regulation of RNA Polymerase I Stability and Function.Cancers · 2022Review
- Ribosome Biogenesis: A Central Player in Cancer Metastasis and Therapeutic Resistance.Cancer research · 2022Review
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- mRNAsi-related genes can effectively distinguish hepatocellular carcinoma into new molecular subtypes.Computational and structural biotechnology journal · 2022Article
- Human rDNA and Cancer.Cells · 2021Review
91 more citing papers are in PubMed but not listed here.
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The tumor suppressor protein p53 is frequently inactivated in tumors. It functions as a transcriptional activator as well as a repressor for a number of viral and cellular promoters transcribed by RNA polymerase II (Pol II) and by RNA Pol III. Moreover, it appears that p53 also suppresses RNA Pol I transcription. In this study, we examined the molecular mechanism of Pol I transcriptional inhibition by p53. We show that wild-type, but not mutant, p53 can repress Pol I transcription from a human rRNA gene promoter in cotransfection assays. Furthermore, we show that recombinant p53 inhibits rRNA transcription in a cell-free transcription system. In agreement with these results, p53-null epithelial cells display an increased Pol I transcriptional activity compared to that of epithelial cells that express p53. However, both cell lines display comparable Pol I factor protein levels. Our biochemical analysis shows that p53 prevents the interaction between SL1 and UBF. Protein-protein interaction assays indicate that p53 binds to SL1, and this interaction is mostly mediated by direct contacts with TATA-binding protein and TAF(I)110. Moreover, template commitment assays show that while the formation of a UBF-SL1 complex can partially relieve the inhibition of transcription, only the assembly of a UBF-SL1-Pol I initiation complex on the rDNA promoter confers substantial protection against p53 inhibition. In summary, our results suggest that p53 represses RNA Pol I transcription by directly interfering with the assembly of a productive transcriptional machinery on the rRNA promoter.
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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.