ArticleBiomedical journal2021
Pristimerin exerts antitumor activity against MDA-MB-231 triple-negative breast cancer cells by reversing of epithelial-mesenchymal transition via downregulation of integrin β3.
Article in Biomedical journal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.
- The Effects of Omega-3 Polyunsaturated Fatty Acids on Breast Cancer as a Preventive Measure or as an Adjunct to Conventional Treatments.Nutrients · 2023Pooled it
- Zeb1 Is a Determinant of EMT in Human MDA-MB-231 Breast Cancer Cells and M13-MDA231 Tumor Hybrids.International journal of molecular sciences · 2026Article
- Molecular Basis of Simalikalactone D Sensitivity in Triple-Negative Breast Cancer Cells.Biomolecules · 2025Article
- Metabolomic Effects and Their Relationship with Intracellular/Extracellular Concentrations of CasiopeinasInternational journal of molecular sciences · 2025Article
- Anticoccidial activity of a botanical natural product based on eucalyptus, apigenin and eugenol against Eimeria tenella in broiler chickens.Parasites & vectors · 2024Article
- Isolation, NMR Characterization, and Bioactivity of a Flavonoid Triglycoside fromAntioxidants (Basel, Switzerland) · 2024Article
- Assessing the impact of extracellular matrix fiber orientation on breast cancer cellular metabolism.Cancer cell international · 2024Article
- Anticancer Potential and Molecular Targets of Pristimerin in Human Malignancies.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Targeting the key players of phenotypic plasticity in cancer cells by phytochemicals.Cancer metastasis reviews · 2024Review
- Pristimerin Exerts Pharmacological Effects Through Multiple Signaling Pathways: A Comprehensive Review.Drug design, development and therapy · 2024Review
- Article
- Modern aspects of the use of natural polyphenols in tumor prevention and therapy.Frontiers in cell and developmental biology · 2022Review
- One day at a time.Biomedical journal · 2021Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPristimerin, a natural flavonoid compound, has potential anti-tumor activities. These activities have been illustrated in various cancer cell lines, including MDA-MB-231 cells. MDA-MB-231 cells are a representative mesenchymal subtype of triple negative breast cancer (MES-TNBC) cell line. Currently, the main treatment for patients with advanced MES-TNBC is cytotoxic chemotherapy. We tried to examine the role and effect of pristimerin on epithelial-mesenchymal transition (EMT) in MDA-MB-231 cells.
methodsThe effects of pristimerin on the proliferation of MDA-MB-231 cells were investigated by cloning formation growth assay. In vitro transwell and adhesion assays were performed for cell invasion and adhesion. The expression levels of EMT markers in E-cadherin and N-cadherin were examined by western blotting. We also established overexpressed- and silenced-integrin β3 cell lines to evaluate the role of integrin β3 in mediating the EMT reversion events in MDA-MB-231 cells.
resultsPristimerin inhibited cell proliferation, and its inhibitory effect was dose-dependent. We demonstrated that pristimerin reserved EMT by upregulating E-cadherin and downregulating N-cadherin expression. Meanwhile, we revealed that pristimerin inhibited mRNA and protein expression of integrin β3, which is a key heterodimeric transmembrane receptor associated with EMT. These inhibitory effects and reversion of EMT were enhanced when integrin β3 was knockdown in MDA-MB-231 cells, while the overexpression of integrin β3 attenuated these effects. In vivo studies using xenograft mouse model demonstrated that pristimerin inhibited tumor growth.
conclusionsOur findings provide important insights into the effects of pristimerin on inhibiting cancer progression and EMT reversion by suppression of integrin β3.
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