ArticleCroatian medical journal2017
The role and possible molecular mechanism of valproic acid in the growth of MCF-7 breast cancer cells.
Article in Croatian medical journal, 2017. 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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Who cites it
16 citing papers in PubMed, 26 citations in OpenAlex.
- Effects of Moringa oleifera extract on biochemical and histological parameters of sodium valproate induced lungs damage.Journal of molecular histology · 2024Article
- Evaluating chemical effects on human neural cells through calcium imaging and deep learning.iScience · 2024Article
- Article
- Effect of valproic acid on histone deacetylase expression in oral cancer (Review).Oncology letters · 2024Review
- Valproate Targets Mammalian Gastrulation Impairing Neural Tissue Differentiation and Development of the Placental Source In Vitro.International journal of molecular sciences · 2022Article
- Epigenetic landscape of drug responses revealed through large-scale ChIP-seq data analyses.BMC bioinformatics · 2022Article
- Reactive Oxygen Species-Mediated Mitochondrial Dysfunction Triggers Sodium Valproate-Induced Cytotoxicity in Human Colorectal Adenocarcinoma Cells.Journal of gastrointestinal cancer · 2021Article
- Effect of valproic acid on miRNAs affecting histone deacetylase in a model of anaplastic thyroid cancer.Molecular biology reports · 2021Article
- Sodium Valproate, a Histone Deacetylase Inhibitor, Provokes Reactive Oxygen Species-Mediated Cytotoxicity in Human Hepatocellular Carcinoma Cells.Journal of gastrointestinal cancer · 2021Article
- Regulation of valproic acid induced EMT by AKT/GSK3β/β-catenin signaling pathway in triple negative breast cancer.Molecular biology reports · 2021Article
- Hyperphosphorylation of HDAC2 promotes drug resistance in a novel dual drug resistant mouse melanoma cell line model: anAmerican journal of cancer research · 2021Article
- Article
- Additive Pharmacological Interaction between Cisplatin (CDDP) and Histone Deacetylase Inhibitors (HDIs) in MDA-MB-231 Triple Negative Breast Cancer (TNBC) Cells with Altered Notch1 Activity-An Isobolographic Analysis.International journal of molecular sciences · 2019Article
- Effect of 5-Aza-2'-Deoxycytidine in Comparison to Valproic Acid and Trichostatin A on Histone Deacetylase 1, DNA Methyltransferase 1, and CIP/KIP Family (p21, p27, and p57) Genes Expression, Cell Growth Inhibition, and Apoptosis Induction in Colon Cancer SW480 Cell Line.Advanced biomedical research · 2019Article
- Mild antagonistic effect of Valproic acid in combination with AZD2461 in MCF-7 breast cancer cells.Medical journal of the Islamic Republic of Iran · 2019Article
- Prolonged Partial Response to Bevacizumab and Valproic Acid in a Patient With Glioblastoma.JCO precision oncology · 2018Article
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
aimTo investigate the role of valproic acid (VPA), a class I selective histone deacetylase inhibitor, on Michigan Cancer Foundation (MCF)-7 breast cancer cells, named and explore its possible molecular mechanism.
methodsMCF-7 cells were cultured with sodium valproate (0. 5-4.0 mmol/L) for 24 h, 48 h, and 72 h in vitro, respectively. The cell viability, apoptosis, and cell cycle were examined. The activities and protein expressions of caspase-3, caspase-8, and caspase-9 were subsequently assayed. Finally, mRNA and protein expressions of cyclin A, cyclin D1, cyclin E, and p21 were analyzed.
resultsSodium valproate suppressed MCF-7 cell growth, induced cell apoptosis, and arrested G1 phase in a time- and concentration- dependent manner, with the relative cell viabilities decreased, cell apoptosis ratios increased, and percentage of G1 phase enhanced (P<0.05). Increased activity of caspase-3 and caspase-9, but not caspase-8, and increased protein levels were found under sodium valproate (2.0 mmol/L, 48h). P21 was up-regulated and cyclin D1 was down-regulated at both mRNA and protein levels under sodium valproate (2.0 mmol/L, 48h)(P<0.05), although cyclin E and cyclin A remained changed.
conclusionThese results indicate that VPA can suppress the growth of breast cancer MCF-7 cells by inducing apoptosis and arresting G1 phase. Intrinsic apoptotic pathway is dominant for VPA-induced apoptosis. For G1 phase arrest, p21 up-regulation and down-regulation of cyclin D1 may be the main molecular mechanism.
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