Betulinic acid and oleanolic acid modulate CD81 expression and induce apoptosis in triple-negative breast cancer cells through ROS generation.

Autor: Lestari DY; Doctoral Program of Medical Science, Faculty of Medicine, Universitas Airlangga, Surabaya, Indonesia.; Medical Faculty, University of Muhammadiyah Malang, Malang, Indonesia., Mastutik G; Department of Pathology Anatomy, Faculty of Medicine, Universitas Airlangga, Surabaya, Indonesia., Mukono IS; Department of Physiology and Medical Biochemistry, Faculty of Medicine, Univesitas Airlangga, Surabaya, Indonesia. indrisafitri@fk.unair.ac.id.
Jazyk: angličtina
Zdroj: Medical oncology (Northwood, London, England) [Med Oncol] 2024 Dec 07; Vol. 42 (1), pp. 24. Date of Electronic Publication: 2024 Dec 07.
DOI: 10.1007/s12032-024-02574-4
Abstrakt: Triple-negative breast cancer (TNBC) is an aggressive subtype of breast cancer characterized by a lack of hormones receptors and the HER2 receptor, making it unresponsive to targeted therapy. Triterpenoids such as betulinic acid (BA) and oleanolic acid (OA) have anticancer effects by inducing apoptosis in TNBC cells. CD81 is a tetraspanin that affects the growth and metastasis of cancer cells. To examine the effect of BA and OA on the viability of TNBC cell line (MDA-MB 231) by analyzing the CD81 expression, intracellular ROS, and apoptosis. The MDA-MB 231 cells was cultured and treated by BA and OA. The viability cell was evaluated by the CCK8 assay. This study analyzed the binding of BA and OA with CD81 using molecular docking and evaluated CD81 expression, intracellular ROS, and apoptosis by flow cytometry. The result showed that BA and OA inhibited viability of MDA-MB-231 cells. BA and OA bind to CD81 in silico, with binding affinities of 9.0 kcal/mol for BA and 7.2 kcal/mol for OA. Flow cytometry results revealed that BA can downregulate CD81 expression. BA and OA also increased intracellular ROS levels and induced apoptosis. These findings suggest that BA and OA, especially BA, can modulate CD81 expression and promote apoptosis in TNBC cells through the generation of ROS, thereby offering a potential therapeutic strategy for the treatment of TNBC.
Competing Interests: Declarations. Conflict of interest: The authors have no relevant financial or non-financial interest to disclose.
(© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)
Databáze: MEDLINE
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