Regulation of E2Fs and senescence by PML nuclear bodies
Open accessAbstract
The tumor suppressor PML (promyelocytic leukemia protein) regulates cellular senescence and terminal differentiation, two processes that implicate a permanent exit from the cell cycle. Here, we show that the mechanism by which PML induces a permanent cell cycle exit and activates p53 and senescence involves a recruitment of E2F transcription factors bound to their promoters and the retinoblastoma (Rb) proteins to PML nuclear bodies enriched in heterochromatin proteins and protein phosphatase 1α. Blocking the functions of the Rb protein family or adding back E2Fs to PML-expressing cells can rescue their defects in E2F-dependent gene expression and cell proliferation, inhibiting the senescent phenotype. In benign prostatic hyperplasia, a neoplastic disease that displays features of senescence, PML was found to be up-regulated and forming nuclear bodies. In contrast, PML bodies were rarely visualized in prostate cancers. The newly defined PML/Rb/E2F pathway may help to distinguish benign tumors from cancers, and suggest E2F target genes as potential targets to induce senescence in human tumors.
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PML and ERK were found in benign human prostatic hyperplasia-derived samples.
“PML and ERK were found in benign human prostatic hyperplasia- derived samples 85,86 .”
From Senescence and cancer — role and therapeutic opportunities (2022) · cites this paper as [85]
The section on PML body formation in benign prostatic hyperplasia (page unavailable) reports stronger PML staining and numerous PML bodies in human BPH samples. The Immunohistochemistry section (page unavailable) describes staining those samples for PML and p16INK4a, but does not report finding ERK in them; a search for ERK found no supporting passage. (LLM, conf=0.90)
Experimental — accuracy not yet measuredPML bodies can be non-exclusive biomarkers of cellular senescence.
“Similarly, PML bodies act as sensors of ROS and oxidative damage (Niwa-Kawakita et al., 2017) and can also be non-exclusive biomarkers of cellular senescence (Vernier et al., 2011).”
From Cellular Senescence: Defining a Path Forward (2019) · cites this paper as Vernier et al., 2011
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- Authors
- Vernier, M., Bourdeau, V., Gaumont-Leclerc, M.-F., Moiseeva, O., Bégin, V., Saad, F., Mes-Masson, A.-M., & Ferbeyre, G.
- Affiliations
- Université de Montréal (CA)
- Venue
- Genes & Development
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2011-01-01
- Volume
- 25
- Issue
- 1
- Pages
- 41-50
- ISSN
- 0890-9369 (ISSN-L)
- 1549-5477
- PMC
- PMC3012935
- OpenAlex
- W2156150950
- Cited by
- 177
- References
- 60
- Citations by year
- 2026: 3 · 2025: 10 · 2024: 6 · 2023: 5 · 2022: 8 · 2021: 10 · 2020: 11 · 2019: 12 · 2018: 17 · 2017: 8 · 2016: 15 · 2015: 11 · 2014: 19 · 2013: 20 · 2012: 14
- Type
- posted content
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Genes & Development (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- HAL (submittedVersion)
- Funders
- Canadian Institutes of Health Research
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Keywords
- PML nuclear bodies, cellular senescence, E2F transcription factors, retinoblastoma protein, p53 activation, cell cycle exit, heterochromatin, benign prostatic hyperplasia, prostate cancer, tumor suppressor, E2F target genes, terminal differentiation
- MeSH terms
- Promyelocytic Leukemia Protein, Cell Nucleus, Gene Expression Regulation, Humans, Male, Nuclear Proteins, Prostatic Hyperplasia, Transcription Factors, Cellular Senescence, Protein Transport, Tumor Suppressor Proteins, Cell Line, Tumor, E2F Transcription Factors
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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