ArticleCell death and differentiation2017
p53 amyloid formation leading to its loss of function: implications in cancer pathogenesis.
Article in Cell death and differentiation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.
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Who cites it
72 citing papers in PubMed, 132 citations in OpenAlex.
- Multi-Site Aggregation of p53: Insights from Self- and Co-Aggregation of Multiple Aggregation-Prone Regions.ACS omega · 2026Article
- Small bites for big problems: stepwise aggregate degradation by autophagy.Biochemical Society transactions · 2026Review
- Cancer-linked aggregation of p53 is driven by sequence-encoded frustration, solvation, and hydrophobic gating absent in its paralogs.Communications chemistry · 2026Article
- The p53 DNA-Binding (Core) Domain can form a prion that seeds prion formation in full-length p53.Microbial cell (Graz, Austria) · 2026Article
- Disease-disease interactions: molecular links of neurodegenerative diseases with cancer, viral infections, and type 2 diabetes.Translational neurodegeneration · 2025Review
- The Evolution of Functional Amyloids and Their Impact on Host-Microbe Interactions.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Molecular targets and therapies associated with poor prognosis of triple‑negative breast cancer (Review).International journal of oncology · 2025Review
- Quantitative diagnosis of amyloid without Congo red staining using polarized light microscopy.Biomedical optics express · 2025Article
- Experimental kinetic mechanism of P53 condensation-amyloid aggregation.Biophysical journal · 2025Article
- Nucleo-cytoplasmic environment modulates spatiotemporal p53 phase separation.Science advances · 2024Article
- Unveiling the multifaceted potential of amyloid fibrils: from pathogenic myths to biotechnological marvels.Biophysical reviews · 2024Review
- Oncogenic p53 triggers amyloid aggregation of p63 and p73 liquid droplets.Communications chemistry · 2024Article
- Impacts of cytoplasmic p53 aggregates on the prognosis and the transcriptome in lung squamous cell carcinoma.Cancer science · 2024Article
- CHEK2 germline variants identified in familial nonmedullary thyroid cancer lead to impaired protein structure and function.The Journal of biological chemistry · 2024Article
- Review
- Physiology and pharmacological targeting of phase separation.Journal of biomedical science · 2024Review
- Amyloid aggregates induced by the p53-R280T mutation lead to loss of p53 function in nasopharyngeal carcinoma.Cell death & disease · 2024Article
- Microbes, macrophages, and melanin: a unifying theory of disease as exemplified by cancer.Frontiers in immunology · 2024Review
- p53 amyloid pathology is correlated with higher cancer grade irrespective of the mutant or wild-type form.Journal of cell science · 2023Article
- Amyloid-like p53 as prognostic biomarker in serous ovarian cancer-a study of the OVCAD consortium.Oncogene · 2023Article
12 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
17 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transcriptional regulator p53 has an essential role in tumor suppression. Almost 50% of human cancers are associated with the loss of p53 functions, where p53 often accumulates in the nucleus as well as in cytoplasm. Although it has been previously suggested that amyloid formation could be a cause of p53 loss-of-function in subset of tumors, the characterization of these amyloids and its structure-function relationship is not yet established. In the current study, we provide several evidences for the presence of p53 amyloid formation (in human and animal cancer tissues); along with its isolation from human cancer tissues and the biophysical characterization of these tissue-derived fibrils. Using amyloid seed of p53 fragment (P8, p53(250-257)), we show that p53 amyloid formation in cells not only leads to its functional inactivation but also transforms it into an oncoprotein. The in vitro studies further show that cancer-associated mutation destabilizes the fold of p53 core domain and also accelerates the aggregation and amyloid formation by this protein. Furthermore, we also show evidence of prion-like cell-to-cell transmission of different p53 amyloid species including full-length p53, which is induced by internalized P8 fibrils. The present study suggests that p53 amyloid formation could be one of the possible cause of p53 loss of function and therefore, inhibiting p53 amyloidogenesis could restore p53 tumor suppressor functions.
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