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Updated: Dec 5, 2025

Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment
Published on: June 9, 2023
Effects of synthetic glucocorticoids on breast cancer progression
Jia Meng Pang1, Yi-Chen Huang2, Shu-Pin Sun3
1Institute of Biotechnology, College of Life Science, National Tsing Hua University, Hsinchu 300, Taiwan; Department of Medical Science, College of Life Science, National Tsing Hua University, Hsinchu 300, Taiwan.
Abstract:
Glucocorticoids (GCs) are widely prescribed as adjuvant therapy for breast cancer patients. Unlike other steroid hormone receptors, the GC receptor is not considered an oncogene. Research in the past few years has revealed the complexity of GC-mediated signaling, but it remains puzzling whether GCs promote or inhibit tumor progression in different cancer types. Here we evaluated the potential of using a synthetic GC, dexamethasone (DEX), in the treatment of breast cancer. We found that the administration of low-dose DEX suppressed tumor growth and distant metastasis in the MCF-7 and MDA-MB-231 xenograft mouse model, whereas treatment with high-dose DEX enhanced tumor growth and metastasis, respectively. Treatment of breast cancer cells with DEX inhibited cell adhesion, migration, and invasion in a dose-dependent manner. The DEX-mediated inhibition of cell adhesion, migration, and invasion is partly through induction of microRNA-708 and subsequent Rap1B-mediated signaling in MDA-MB-231 cells. On the other hand, in MCF-7 cells, DEX-suppressed cell migration is independent from microRNA-708 mediated signaling. Overall, our data reveal that DEX acts as a double-edged sword during breast-cancer progression and metastasis: Lower concentrations inhibit breast cancer tumor growth and metastasis, whereas higher concentrations may play an undesired role to promote breast cancer progression.
Insights
Glucocorticoids (GCs), like dexamethasone (DEX), show dual effects in breast cancer. Low-dose DEX inhibits tumor growth and metastasis, while high-dose DEX may promote cancer progression.
Area of Science:
- Oncology
- Endocrinology
- Molecular Biology
Background:
- Glucocorticoids (GCs) are commonly used in breast cancer treatment.
- The role of GCs in tumor progression is complex and not fully understood.
- Dexamethasone (DEX), a synthetic GC, is evaluated for its therapeutic potential.
Purpose of the Study:
- To investigate the dose-dependent effects of dexamethasone (DEX) on breast cancer growth, metastasis, and cell behavior.
- To elucidate the underlying molecular mechanisms of DEX action in different breast cancer cell lines.
Main Methods:
- Utilized MCF-7 and MDA-MB-231 xenograft mouse models to assess tumor growth and metastasis.
- Administered varying doses of DEX to evaluate its impact on cancer cell adhesion, migration, and invasion.
- Investigated the role of microRNA-708 and Rap1B signaling in mediating DEX effects.
Main Results:
- Low-dose DEX suppressed tumor growth and metastasis in vivo.
- High-dose DEX enhanced tumor growth and metastasis in vivo.
- DEX inhibited cell adhesion, migration, and invasion in a dose-dependent manner.
- DEX-mediated inhibition involved microRNA-708 and Rap1B signaling in MDA-MB-231 cells, but not in MCF-7 cells.
Conclusions:
- Dexamethasone exhibits a dose-dependent, double-edged sword effect in breast cancer.
- Low concentrations of DEX may be beneficial for inhibiting tumor progression and metastasis.
- High concentrations of DEX could potentially promote breast cancer progression, warranting careful clinical consideration.
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