ArticleCancer science2018
Simvastatin functions as a heat shock protein 90 inhibitor against triple-negative breast cancer.
Article in Cancer science, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 2 of them syntheses that pooled it.
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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
22 citing papers in PubMed, 2 syntheses or guidelines pooled it, 37 citations in OpenAlex.
- The Influence of Statin Use on Chemotherapeutic Efficacy in Studies of Mouse Models: A Systematic Review.Anticancer research · 2023Pooled it
- Signaling Pathways and Natural Compounds in Triple-Negative Breast Cancer Cell Line.Molecules (Basel, Switzerland) · 2022Pooled it
- Screening of signaling pathways and hub genes in Guillain-Barré syndrome based on bioinformatics and machine learning.BMC neurology · 2026Article
- Article
- Repurposing a Lipid-Lowering Agent to Inhibit TNBC Growth Through Cell Cycle Arrest.Current issues in molecular biology · 2025Article
- Comprehensive pan-cancer analysis of NLRs family as prognostic and immunity markers based on multi-omics data.Discover oncology · 2025Article
- Comprehensive pan-cancer analysis of FUTs family as prognostic and immunity markers based on multi-omics data.Discover oncology · 2024Article
- Simvastatin, Its Antimicrobial Activity and Its Prevention of Alzheimer's Disease.Microorganisms · 2024Review
- Comprehensive pan-cancer analysis of inflammatory age-clock-related genes as prognostic and immunity markers based on multi-omics data.Scientific reports · 2024Article
- Mutant p53 murine oviductal epithelial cells induce progression of high-grade serous carcinoma and are most sensitive to simvastatin therapy in vitro and in vivo.Journal of ovarian research · 2023Article
- Post-diagnostic statin use and breast cancer-specific mortality: a population-based cohort study.Breast cancer research and treatment · 2023Article
- Review
- Smell Detection Agent Optimisation Framework and Systems Biology Approach to Detect Dys-Regulated Subnetwork in Cancer Data.Biomolecules · 2021Article
- Association of statin use with clinical outcomes in patients with triple-negative breast cancer.Cancer · 2021Article
- Review
- CDC37L1 acts as a suppressor of migration and proliferation in gastric cancer by down-regulating CDK6.Journal of Cancer · 2021Article
- Systems pharmacology in combination with proteomics reveals underlying mechanisms of Xihuang pill against triple-negative breast cancer.Bioengineered · 2020Article
- Prodigiosin/PU-H71 as a novel potential combined therapy for triple negative breast cancer (TNBC): preclinical insights.Scientific reports · 2020Article
- Targeting SREBP-2-Regulated Mevalonate Metabolism for Cancer Therapy.Frontiers in oncology · 2020Review
- STAT3 and mutp53 Engage a Positive Feedback Loop Involving HSP90 and the Mevalonate Pathway.Frontiers in oncology · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
Acetylation plays an important role in regulating the chaperone activity of heat shock protein 90 (Hsp90) during malignant transformation through the stabilization and conformational maturation of oncogenic proteins. However, the functional acetylation sites, potential anticancer drug targets, are still emerging. We found that acetylation at K292 in Hsp90α is critical for the development and treatment of breast cancer. Acetylation at K292 not only augments the affinity of Hsp90 to ATP, cochaperones, and client proteins but it also promotes cancer cell colony formation, migration, and invasion in vitro as well as tumor growth in vivo. Importantly, K292-acetylated Hsp90 has been validated as an exciting anticancer drug target by interfering with the complex formation between K292-acetylated Hsp90 and cochaperone Cdc37, leading to diminishment of kinase client maturation and proteasome-dependent degradation of kinase substrates. Furthermore, we showed that simvastatin prevented, whereas LBH589 promoted, the progression of Hsp90 chaperone cycling and client maturation, resulting in an increment of cell apoptosis by the combination of simvastatin and LBH589 in a mouse xenograft model. These data suggest that simvastatin is a novel Hsp90 inhibitor to disrupt the formation of the K292-acetylated Hsp90/Cdc37 complex in triple-negative breast cancer cells. The combination of simvastatin with LBH589 could be used as a novel therapeutic strategy for triple-negative breast cancer.
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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.