ArticlePloS one2018
Lipophilic statins limit cancer cell growth and survival, via involvement of Akt signaling.
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 5 of them syntheses that pooled it.
What it found
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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
61 citing papers in PubMed, 5 syntheses or guidelines pooled it, 120 citations in OpenAlex.
- Statin Use and Hepatocellular Carcinoma Risk: A Comprehensive Meta-Analysis and Systematic Review.Recent patents on anti-cancer drug discovery · 2025Pooled it
- Association between Statin Use and Chemotherapy-Induced Cardiotoxicity: A Meta-Analysis.Medicina (Kaunas, Lithuania) · 2024Pooled it
- Pooled it
- Systematic review and meta-analysis of studies assessing the relationship between statin use and risk of ovarian cancer.Cancer causes & control : CCC · 2020Pooled it
- Do statins play any role in reducing the incidence and mortality of ovarian cancer? A systematic review and meta-analysis.Journal of preventive medicine and hygiene · 2020Pooled it
- Dyslipidaemias in cancer patients.European heart journal · 2026Review
- Emerging roles of the metabolic regulator 3-hydroxy-3-methylglutaryl coenzyme-CoA reductase in human cancers: From biology to therapeutics.Genes & diseases · 2026Review
- The impact of statins on prognostic outcomes in patients with non-metastatic solid cancers: a systematic review and meta-analysis.Discover oncology · 2026Review
- Repurposing statins for choriocarcinoma: targeting the mevalonate pathway to disrupt mechanosignaling and overcome therapeutic resistance.Clinical & experimental metastasis · 2026Review
- Enhancing the Water Solubility and Efficacy of Anticancer Drugs Using Hydroxypropyl-β-Cyclodextrin.International journal of molecular sciences · 2026Review
- Combined Effects of Atorvastatin and Glucose Deprivation on Metabolic Stress and Lipid-Raft Disruption in Glioblastoma and Breast Cancer Cells.Pharmaceutics · 2025Article
- In Vitro Investigation of the Antiproliferative and Antimetastatic Effects of Atorvastatin: A Focus on Cervical and Head and Neck Cancers.Pharmaceutics · 2025Article
- Effects of Statins on All-Cause Mortality in Patients with Breast Cancer: A Population-Based Study.Biomedicines · 2025Article
- Molecular mechanisms underlying the effects of statins on bone metabolism: an evolving paradigm of statins delivery modalities for bone regeneration.Pharmacological reports : PR · 2025Review
- Statins as Secondary Preventive Agent to Limit Breast Cancer Metastatic Outgrowth.International journal of molecular sciences · 2025Review
- The effect and mechanism of atorvastatin regulating PI3K-Akt-mTOR pathway on radiosensitivity of hepatocellular carcinoma cells.Toxicology research · 2025Article
- Statins regulate kinase signaling by causing changes in phosphorylation, rather than through changes in gene expression or direct inhibition: evidence in colorectal cancer.Frontiers in pharmacology · 2025Article
- Targeting Cholesterol Biosynthesis with Statins Synergizes with AKT Inhibitors in Triple-Negative Breast Cancer.Cancer research · 2024Article
- The Effect of Statins on Markers of Breast Cancer Proliferation and Apoptosis in Women with In Situ or Early-Stage Invasive Breast Cancer.International journal of molecular sciences · 2024Article
- Effect of Statin Lipophilicity on the Proliferation of Hepatocellular Carcinoma Cells.Biology · 2024Article
1 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 1 institution in 1 country.
Funding
Abstract
The HMG-CoA reductase inhibitors, statins, have been used as lipid lowering drugs for decades and several epidemiological studies suggest statin usage correlates with a decreased incidence of cancer specific mortality in patients. However, the mechanism of this mortality benefit remains unclear. Here, we demonstrate that statin drug lipophilicity and affinity for its target enzyme, HMGCR, determine their growth suppressive potency against various tumor cell lines. The lipophilic atorvastatin decreases cancer cell proliferation and survival in vitro. Statin sensitivity coincided with Ras localization to the cytosol instead of the membrane, consistent with a decrement in prenylation. To investigate signaling pathways that may be involved with sensitivity to statin therapy, we employed inhibitors of the PI3K-Akt and Mek-Erk signaling cascades. We found that inhibition of PI3K signaling through Akt potentiated statin sensitivity of breast cancer cells in vitro and in co-culture with primary human hepatocytes. The same effect was not observed with inhibition of Mek signaling through Erk. Moreover, the sensitivity of breast cancer cells to atorvastatin-mediated growth suppression correlated with a decrease in EGF-mediated phosphorylation of Akt. As an increase in Akt activity has been shown to be involved in the metastasis and metastatic outgrowth of many cancer types (including breast), these data suggest a mechanism by which statins may reduce cancer specific mortality in patients.
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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.