ReviewCell death and differentiation2018
The interplay between mutant p53 and the mevalonate pathway.
Review in Cell death and differentiation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 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
68 citing papers in PubMed, 97 citations in OpenAlex.
- Revisiting tumor immunogenicity through the lens of mutant p53: Implications for cancer immunotherapy.Apoptosis : an international journal on programmed cell death · 2026Review
- Liquid Biopsy-Based Metabolomics in Epithelial Ovarian Cancer: Challenges, Methodological Advances and Translational Considerations.Diagnostics (Basel, Switzerland) · 2026Review
- Medulloblastoma response to mevalonate pathway inhibition is independent of p53 status.Biology direct · 2026Article
- Wnt ligands in breast cancer metastasis: unraveling their dual roles and therapeutic potential.Molecular biology reports · 2026Review
- Metabolic remodeling and immune evasion in glioblastoma: a focus on serine and lipid networks.Frontiers in oncology · 2026Review
- Towards Post-Genomic Oncology: Embracing Cancer Complexity via Artificial Intelligence, Multi-Targeted Therapeutics, Drug Repurposing, and Innovative Study Designs.International journal of molecular sciences · 2025Review
- DNAJA: emerging targets for anti-tumor therapy.Future oncology (London, England) · 2025Review
- Transcriptomic Insights Into Serum-Free Medium Adaptation and Temperature Reduction in Chinese Hamster Ovary Cell Cultures.Biotechnology journal · 2025Article
- Chemoproteomics reveals proteome-wide covalent and non-covalent targets of withaferin A.Acta pharmacologica Sinica · 2025Article
- Statins and the Risk of Colorectal Cancer in Patients With Inflammatory Bowel Disease: A Systematic Review and Meta-Analysis.Gastroenterology research · 2025Article
- Mammalian Ste20-like kinase 1 regulates AMPK to mitigate the progression of non-alcoholic fatty liver disease.European journal of medical research · 2025Article
- Review
- In vivo CRISPR screening identifies geranylgeranyl diphosphate as a pancreatic cancer tumor growth dependency.Molecular metabolism · 2024Article
- Prediction of metabolites associated with somatic mutations in cancers by using genome-scale metabolic models and mutation data.Genome biology · 2024Article
- TP53 to mediate immune escape in tumor microenvironment: an overview of the research progress.Molecular biology reports · 2024Review
- Review
- Mutant p53 in head and neck squamous cell carcinoma: Molecular mechanism of gain‑of‑function and targeting therapy (Review).Oncology reports · 2023Review
- Etiological relationship between lipid metabolism and endometrial carcinoma.Lipids in health and disease · 2023Review
- Mutant APC reshapes Wnt signaling plasma membrane nanodomains by altering cholesterol levels via oncogenic β-catenin.Nature communications · 2023Article
- Review
8 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Missense mutations in the TP53 gene lead to accumulation of dysfunctional TP53 proteins in tumors, showing oncogenic gain-of-function (GOF) activities. Stabilization of mutant TP53 (mutp53) is required for the GOF; however, the mechanisms by which mutp53 promotes cancer progression and how mutp53 stability is regulated are not completely understood. Recent work from our laboratory has identified statins, inhibitors of the mevalonate pathway, as degraders of conformational mutp53. Specific reduction of mevalonate-5-phosphate (MVP), a metabolic intermediate in the mevalonate pathway, by statins or mevalonate kinase (MVK) knockdown triggers CHIP ubiquitin ligase-mediated degradation of conformational mutp53 by inhibiting interaction between mutp53 and DNAJA1, a Hsp40 family member. Thus, the mevalonate pathway contributes to mutp53 stabilization. Given that mutp53 is shown to promote cancer progression by upregulating mRNA expression of mevalonate pathway enzymes by binding to the sterol regulatory element-binding protein 2 (SREBP2) and subsequently increasing activities of mevalonate pathway-associated oncogenic proteins (e.g., Ras, Rho, YAP/TAZ), there is a positive-feedback loop between mutp53 and the mevalonate pathway. Here, we summarize recent evidence linking the mevalonate pathway-mutp53 axis with cancer progression and further discuss the clinical relevance of this axis.
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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.