Related Experiment Video
Updated: Jun 5, 2025

Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment
Published on: June 9, 2023
Betulinic acid and oleanolic acid modulate CD81 expression and induce apoptosis in triple-negative breast cancer
Dian Yuliartha Lestari1,2, Gondo Mastutik3, Indri Safitri Mukono4
1Doctoral Program of Medical Science, Faculty of Medicine, Universitas Airlangga, Surabaya, Indonesia.
Betulinic acid (BA) and oleanolic acid (OA) show promise for treating triple-negative breast cancer (TNBC). These compounds inhibit cancer cell viability by increasing ROS and apoptosis, with BA also downregulating CD81 expression.
Area of Science:
- Molecular Biology
- Cancer Research
- Pharmacology
Background:
- Triple-negative breast cancer (TNBC) lacks hormone and HER2 receptors, limiting treatment options.
- Triterpenoids like betulinic acid (BA) and oleanolic acid (OA) exhibit anticancer properties.
- CD81, a tetraspanin, influences cancer cell growth and metastasis.
Purpose of the Study:
- To investigate the effects of BA and OA on MDA-MB-231 TNBC cell viability.
- To analyze the impact of BA and OA on CD81 expression, intracellular ROS, and apoptosis.
- To explore the potential therapeutic role of BA and OA in TNBC treatment.
Main Methods:
- Cell culture and treatment of MDA-MB-231 cells with BA and OA.
- Cell viability assessment using the CCK8 assay.
- Molecular docking to analyze BA and OA binding to CD81.
- Flow cytometry to evaluate CD81 expression, intracellular ROS, and apoptosis.
Main Results:
- BA and OA significantly inhibited the viability of MDA-MB-231 cells.
- Molecular docking revealed binding affinities of -9.0 kcal/mol for BA-CD81 and -7.2 kcal/mol for OA-CD81.
- BA treatment downregulated CD81 expression.
- Both BA and OA increased intracellular ROS levels and induced apoptosis in TNBC cells.
Conclusions:
- BA and OA demonstrate efficacy in reducing TNBC cell viability.
- These triterpenoids promote apoptosis and increase ROS generation in cancer cells.
- BA's ability to modulate CD81 expression suggests a specific mechanism in TNBC treatment, offering a potential therapeutic strategy.
More Related Videos
19:44Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen
Published on: May 30, 2012
06:54Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
Published on: October 27, 2020