ArticleEMBO molecular medicine2024
PML restrains p53 activity and cellular senescence in clear cell renal cell carcinoma.
Article in EMBO molecular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- Nuclear PML expression as a prognostic biomarker in localised clear cell renal cell carcinoma.BJUI compass · 2026Article
- A single chromosome 3p break initiates clear cell renal cell carcinoma evolution.bioRxiv : the preprint server for biology · 2026Article
- TMEM72 Inhibits the proliferation by promoting cellular senescence through the activation of the P38/MAPK signaling pathway in renal cell carcinoma.Translational oncology · 2026Article
- NAT10-mediated N4-acetylcytidine modification drives RNA splicing of PML to alleviate adipose-derived stem cell senescence and promote diabetic wound healing.Clinical and translational medicine · 2026Article
- The tumor promoter role and molecular mechanism of C8orf76/CALB2 axis in clear cell renal cell carcinoma.iScience · 2026Article
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- Regulation of ribosomal gene expression and senescence by a PML-mTOR-RONIN nuclear complex in triple-negative breast cancer.Oncogene · 2025Article
- Kaempferol triggers cellular senescence via CDK1 ubiquitination in HCC cells.Cancer cell international · 2025Article
- Design principles of gene circuits for longevity.Trends in cell biology · 2025Review
- Cellular senescence in cancer: from mechanism paradoxes to precision therapeutics.Molecular cancer · 2025Review
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Authors and funding
12 authors.
Funding
Abstract
Clear-cell renal cell carcinoma (ccRCC), the major subtype of RCC, is frequently diagnosed at late/metastatic stage with 13% 5-year disease-free survival. Functional inactivation of the wild-type p53 protein is implicated in ccRCC therapy resistance, but the detailed mechanisms of p53 malfunction are still poorly characterized. Thus, a better understanding of the mechanisms of disease progression and therapy resistance is required. Here, we report a novel ccRCC dependence on the promyelocytic leukemia (PML) protein. We show that PML is overexpressed in ccRCC and that PML depletion inhibits cell proliferation and relieves pathologic features of anaplastic disease in vivo. Mechanistically, PML loss unleashed p53-dependent cellular senescence thus depicting a novel regulatory axis to limit p53 activity and senescence in ccRCC. Treatment with the FDA-approved PML inhibitor arsenic trioxide induced PML degradation and p53 accumulation and inhibited ccRCC expansion in vitro and in vivo. Therefore, by defining non-oncogene addiction to the PML gene, our work uncovers a novel ccRCC vulnerability and lays the foundation for repurposing an available pharmacological intervention to restore p53 function and chemosensitivity.
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Registered trials
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