ArticlePharmaceutical biology2024
Tabersonine enhances cisplatin sensitivity by modulating Aurora kinase A and suppressing epithelial-mesenchymal transition in triple-negative breast cancer.
Article in Pharmaceutical biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- RBM15B-mediated m6A modification of FOXM1 activates the AURKA/TPX2 axis to promote epithelial-mesenchymal transition-driven endometrial cancer progression.Cell adhesion & migration · 2026Article
- Ginsenoside Rh2 inhibits non-small-cell lung cancer malignant progression through targeting AURKA.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Cyclic Imines and Their Salts as Universal Precursors in the Synthesis of Nitrogen-Containing Alkaloids.International journal of molecular sciences · 2024Review
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
contextTabersonine has been investigated for its role in modulating inflammation-associated pathways in various diseases. However, its regulatory effects on triple-negative breast cancer (TNBC) have not yet been fully elucidated.
objectiveThis study uncovers the anticancer properties of tabersonine in TNBC cells, elucidating its role in enhancing chemosensitivity to cisplatin (CDDP). MATERIALS AND
methodsAfter tabersonine (10 μM) and/or CDDP (10 μM) treatment for 48 h in BT549 and MDA-MB-231 cells, cell proliferation was evaluated using the cell counting kit-8 and colony formation assays. Quantitative proteomics, online prediction tools and molecular docking analyses were used to identify potential downstream targets of tabersonine. Transwell and wound-healing assays and Western blot analysis were used to assess epithelial-mesenchymal transition (EMT) phenotypes.
resultsTabersonine demonstrated inhibitory effects on TNBC cells, with IC DISCUSSION AND
conclusionsTabersonine significantly enhances the chemosensitivity of CDDP in TNBC cells, underscoring its potential as a promising therapeutic agent for TNBC treatment.
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