ArticleToxicology research2020
Enhanced apoptogenesis and oncogene regulatory mechanism of troxerutin in triple negative breast cancer cells.
Article in Toxicology research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 15 citations in OpenAlex.
- Molecular insights into triazole-based compounds for triple-negative breast cancer treatment.Journal of enzyme inhibition and medicinal chemistry · 2026Review
- Extracellular vesicle delivery of Myricetin suppresses ovarian cancer through mitochondrial dynamics by downregulating the ECM1/NF-κB/TGFβ signaling pathway.Scientific reports · 2026Article
- Mechanism of action for Troxerutin targeting the sialylation-related gene EGLN3 for the treatment of LUAD.Scientific reports · 2025Article
- Targeting Ferroptosis as a Therapeutic Implication in Lung Cancer Treatment by a Novel Naphthoquinone Inducer: Juglone.Molecular biotechnology · 2024Article
- An Insight on Synergistic Anti-cancer Efficacy of Biochanin A and Sulforaphane Combination Against Breast Cancer.Applied biochemistry and biotechnology · 2024Article
- The therapeutic effect of traditional Chinese medicine on breast cancer through modulation of the Wnt/β-catenin signaling pathway.Frontiers in pharmacology · 2024Review
- Zinc-finger protein 382 antagonises CDC25A and ZEB1 signaling pathway in breast cancer.Genes & diseases · 2023Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Triple negative breast carcinoma (TNBC) is an aggressive form of cancer, with high rates of morbidity, mortality, poor prognosis and limited therapeutic options. The objective of the present study was to elaborate the anticancer activity of Troxerutin (TXN) in TNBC/MDA-MB-231 cells. Herein, we demonstrated the inhibitory effects of TXN on the breast cancer cell growth via induction of apoptosis. Mitochondrial membrane potential (∆Ψm), DNA damage and apoptotic nuclear changes were analyzed by flowcytometry, AO/EtBr and Hoechst staining, respectively. Furthermore, apoptotic protein and gene expressions were analyzed by western blot and reverse transcription polymerase chain reaction (RT-PCR), respectively. Our results indicated that TXN induces apoptosis as evidenced by inhibit the cell proliferation, enhanced apoptotic activation, altered mitochondrial membrane potential and elevated level of DNA damage in TNBC cells. Furthermore, the TXN inhibit anti-apoptotic protein expression with the subsequent upregulation of Cytochrome c, Caspase-9 and Caspase-3. Thus, TXN induces apoptosis in TNBC cells through inducing nuclear damage and altered apoptotic marker expressions. Therefore, TXN might be used as a potential therapeutic agent for the treatment of triple negative breast cancer.
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