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Enhancement radiosensitization of breast cancer cells by deguelin
Tongbo Yi1, Haizhi Li, Xuanyi Wang
1Department of Breast and Endocrine Surgery, The First Affiliated Hospital, Nanjing Medical University, Nanjing, Jiangsu Province, China.
Objective:
Radiation can activate the phosphatidylinositol 3-kinase/Akt pathway and cannot downregulate survivin expression in breast cancer cells. Deguelin induces apoptosis in breast cancer cells by inhibiting pAkt and survivin expression. In this study, we assessed the effect of deguelin on radiosensitization of human breast cancer cells and its possible mechanism.
Methods:
Deguelin and radiation were administrated in MDA-MB-231 human breast cancer cells. The cytotoxic interactions and mutual influences between these 2 modalities were analyzed by a series of assays including clonogenic, flow cytometric, and Western blotting.
Results:
Phospho-Akt expression and survivin expression significantly decreased after 10 nM deguelin treatment, while phospho-Akt expression increased and survivin expression did not alter after radiation (3 Gy). However, phospho-Akt expression and survivin expression further significantly decreased after deguelin combined with radiation treatment. Deguelin combined with radiation markedly decreased clonogenic cell survival. After treatment of deguelin (10 nM) combined with radiation (3 Gy), caspase-dependent apoptosis was significantly increased and cell cycle was arrested in the G2-M phase in MDA-MB-231 cells.
Conclusions:
Deguelin attenuates radiation-induced prosurvival Akt signaling and enhances the radiosensitivity of MDA-MB-231 cells, and the mechanisms for this action may include inhibiting phospho-Akt and survivin expression, increasing caspase-dependent apoptosis, and prolonging cell cycle arrest in the G2-M phase.
Insights
Deguelin enhances radiation therapy effectiveness in breast cancer by inhibiting pro-survival pathways like Akt and survivin. This combination therapy increases apoptosis and cell cycle arrest, improving treatment outcomes.
Area of Science:
- Oncology
- Molecular Biology
- Radiotherapy
Background:
- Radiation therapy can activate the phosphatidylinositol 3-kinase/Akt pathway, promoting breast cancer cell survival.
- Survivin expression is often upregulated in breast cancer, contributing to treatment resistance.
- Deguelin is known to induce apoptosis by inhibiting phospho-Akt (pAkt) and survivin.
Purpose of the Study:
- To investigate the radiosensitizing effect of deguelin on human breast cancer cells (MDA-MB-231).
- To elucidate the underlying mechanisms of deguelin-mediated radiosensitization.
Main Methods:
- MDA-MB-231 cells were treated with deguelin and/or radiation (3 Gy).
- Cytotoxic interactions were assessed using clonogenic assays.
- Apoptosis and cell cycle progression were analyzed by flow cytometry.
- Expression levels of pAkt and survivin were determined by Western blotting.
Main Results:
- Deguelin (10 nM) alone decreased pAkt and survivin expression.
- Radiation alone increased pAkt expression and did not alter survivin expression.
- Combined deguelin and radiation significantly decreased pAkt and survivin expression.
- The combination treatment markedly reduced clonogenic cell survival.
- Deguelin plus radiation significantly increased caspase-dependent apoptosis and induced G2-M cell cycle arrest.
Conclusions:
- Deguelin enhances the radiosensitivity of MDA-MB-231 breast cancer cells.
- Deguelin attenuates radiation-induced pro-survival Akt signaling.
- Mechanisms include inhibition of pAkt and survivin, increased apoptosis, and prolonged G2-M cell cycle arrest.
