ArticleScientific reports2022
Systematic understanding of anti-tumor mechanisms of Tamarixetin through network and experimental analyses.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- Photophysical Investigation of Coumarin Solubilization in Polyethylene Glycol Mediated by a 1,2,4-Triazolium Protic Ionic Liquid.ACS omega · 2026Article
- Advances in quercetin-based therapeutics for breast cancer: natural, synthetic, and nanotechnology-driven approaches.Medicinal chemistry research : an international journal for rapid communications on design and mechanisms of action of biologically active agents · 2026Review
- Tamarixetin Suppresses Colorectal Cancer Progression by Targeting DPP7-Mediated WNT3A/β-Catenin Signalling Pathway.Journal of cellular and molecular medicine · 2025Article
- Research Progress of Tamarixetin and its Glycosides.Mini reviews in medicinal chemistry · 2024Review
- Ninety-six-hour starved peripheral blood mononuclear cell supernatant inhibited LA7 breast cancer stem cells induced tumorFrontiers in immunology · 2022Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tamarixetin, a flavonoid derived from Quercetin, was shown to possess anti-cancer properties in various types of cancer. However, the mechanism of action of this compound is not well understood. Observations from reverse docking and network pharmacology analysis, were validated by cell based studies to analyse the chemotherapeutic potential and elucidate the molecular mechanism of action of Tamarixetin in breast cancer. In silico analysis using reverse docking and PPI analysis clearly indicated that out of 35 proteins targeted by Tamarixetin, the top 3 hub genes, namely, AKT1, ESR1 and HSP90AA1, were upregulated in breast tumor tissues and more importantly showed strong negative correlation to breast cancer patient survival. Furthermore, the KEGG pathway analysis showed enrichment of target proteins of Tamarixetin in 33 pathways which are mainly involved in neoplastic signalling. In vitro cell-based studies demonstrated that Tamarixetin could inhibit cell proliferation, induce ROS and reduce mitochondrial membrane potential, leading to cell death. Tamarixetin induced cell cycle arrest at G2/M phase and inhibited the migration as well as the invasion of breast cancer cells. Taken together, the combination of in silico and in vitro approaches used in the present study clearly provides evidence for the chemotherapeutic potential of Tamarixetin in breast cancer.
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