ArticleOncology letters2016
Simvastatin blocks TGF-β1-induced epithelial-mesenchymal transition in human prostate cancer cells.
Article in Oncology letters, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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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.
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Who cites it
16 citing papers in PubMed, 37 citations in OpenAlex.
- Cholesterol-Lowering Treatment Blocks Epithelial-Mesenchymal Transition (EMT) Associated Invasiveness and Drug Resistance in Breast and Colorectal Adenocarcinoma Models.Cancer medicine · 2026Article
- FAM107A inhibits Invasion and migration of colorectal cancer by affecting EMT via the AKT pathway.Histology and histopathology · 2026Article
- FBXO28 promotes cell proliferation, migration and invasion via upregulation of the TGF-beta1/SMAD2/3 signaling pathway in ovarian cancer.BMC cancer · 2024Article
- Simvastatin alleviates epithelial-mesenchymal transition and oxidative stress of high glucose-induced lens epithelial cellsExperimental and therapeutic medicine · 2022Article
- Polyploid giant cancer cells are dependent on cholesterol for progeny formation through amitotic division.Scientific reports · 2022Article
- Statins affect cancer cell plasticity with distinct consequences for tumor progression and metastasis.Cell reports · 2021Article
- Review
- Role of Cadherins in Cancer-A Review.International journal of molecular sciences · 2020Review
- Inhibitory effect of endostar combined with radiotherapy on gastric cancer animal models.World journal of surgical oncology · 2020Article
- Atorvastatin and Caffeine in Combination Regulates Apoptosis, Migration, Invasion and Tumorspheres of Prostate Cancer Cells.Pathology oncology research : POR · 2020Article
- Restoring E-cadherin Expression by Natural Compounds for Anticancer Therapies in Genital and Urinary Cancers.Molecular therapy oncolytics · 2019Review
- Curbing Lipids: Impacts ON Cancer and Viral Infection.International journal of molecular sciences · 2019Review
- Inflammatory Proteomic Network Analysis of Statin-treated and Lipopolysaccharide-activated Macrophages.Scientific reports · 2018Article
- The effect of mast cells on the biological characteristics of prostate cancer cells.Central-European journal of immunology · 2018Article
- Cholesterol overload in the liver aggravates oxidative stress-mediated DNA damage and accelerates hepatocarcinogenesis.Oncotarget · 2017Article
- Identification of simvastatin-regulated targets associated with JNK activation in DU145 human prostate cancer cell death signaling.BMB reports · 2017Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In recent years, the use of statins has been reported to be associated with a reduced risk of prostate cancer (PCa), particularly metastatic PCa. The mechanisms underlying these epidemiological observations are poorly understood. Epithelial-mesenchymal transition (EMT) is a critical initial step and a hallmark for cancer metastasis. In the present study, the relationship between simvastatin and EMT in PCa and the mechanism involved was investigated. It was demonstrated that simvastatin inhibited the EMT as assessed by reduced expression of N-cadherin and vimentin, and increased E-cadherin in TGF-β1 treated DU145 PCa cells. Furthermore, simvastatin inhibited TGF-β1-induced migration and invasion of DU145 cells. The TGF-β1/Smad pathway and non-Smad pathway were investigated in simvastatin-treated DU145 cells. Simvastatin had no effect on TGF-β1-induced phosphorylation of Smad2 and Smad3. In the non-Smad pathway, simvastatin reduced TGF-β1-induced p38 MAPK phosphorylation, but had no effect on TGF-β1-induced Erk1/2 phosphorylation. Simvastatin attenuated TGF-β1-induced EMT, cell migration and invasion in DU145 cells. These effects may have been mediated by the inhibition of p38 MAPK phosphorylation, not through the canonical Smad pathway. Therefore simvastatin may be a promising therapeutic agent for treating PCa.
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