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SBFI-26 enhances apoptosis in docetaxel-treated triple-negative breast cancer cells by increasing ROS levels
Gang He1,2, Mei Liu1, Tang Cong Chen1
1Key Laboratory of Medicinal and Edible Plants Resources Development of Sichuan Education Department, Sichuan Industrial Institute of Antibiotics, School of Pharmacy, Chengdu University, Chengdu, China.
Introduction:
Fatty acid binding protein 5 (FABP5) exhibits heightened expression levels in triple-negative breast cancer. The inhibitor of FABP5, Stony Brook fatty acid-binding protein inhibitor 26 (SBFI-26), has demonstrated the capacity to suppress cell proliferation, migration, and invasion. This study delves into the functional mechanism and impact of combining SBFI-26 with docetaxel in treating MDA-MB-231 cells of triple-negative breast cancer.
Methods:
Various concentrations of docetaxel and SBFI-26 were chosen for individual or combined treatments. The effects of SBFI-26, docetaxel, or their combination on cell cycle arrest and apoptosis were assessed using flow cytometry. Western blotting was utilised to detect the expression of apoptosis-related proteins, namely cysteinyl aspartate-specific proteases 3 (Caspase3), B cell leukemia/lymphoma 2 (Bcl-2), and Bcl-2 associated X (Bax), while intracellular reactive oxygen species (ROS) levels were determined using a fluorescence spectrophotometer.
Results:
The IC50 values for SBFI-26 and docetaxel in inhibiting MDA-MB-231 cells were determined to be 106.1 μM and 86.14 nM, respectively. Significantly, the combination treatment augmented the proportion of G1 phase (apoptotic) cells by 3.67-fold compared to the control group (P < 0.0001). Furthermore, the apoptosis rate in the combination group was 2.59-fold higher than that in the docetaxel group (P < 0.0001) and demonstrated a significant increase of 1.82-fold compared with the SBFI-26 group (P < 0.001). Analyses revealed a decrease in the protein expression of Bcl-2, while Bax and Caspase3 exhibited an increase in the combination group for MDA-MB-231 cells. Moreover, the combined treatment group demonstrated a 2.97-fold increase (P < 0.0001) in ROS fluorescence intensity compared to the control group, a noteworthy 1.39-fold increase (P < 0.01) compared to the SBFI-26 treatment group, and a substantial 1.70-fold increase (P < 0.0001) compared to the docetaxel treatment group.
Conclusion:
These findings suggest that the co-administration of SBFI-26 with docetaxel effectively enhances apoptosis in triple-negative breast cancer MDA-MB-231 cells by elevating intracellular ROS levels.
Insights
Combining Stony Brook fatty acid-binding protein inhibitor 26 (SBFI-26) with docetaxel significantly enhances apoptosis in triple-negative breast cancer cells. This combination therapy increases reactive oxygen species (ROS) levels, offering a promising strategy for MDA-MB-231 cell treatment.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Fatty acid binding protein 5 (FABP5) is overexpressed in triple-negative breast cancer (TNBC).
- SBFI-26, a FABP5 inhibitor, suppresses proliferation, migration, and invasion of cancer cells.
- TNBC remains a challenging subtype of breast cancer with limited targeted therapies.
Purpose of the Study:
- To investigate the combined effect of SBFI-26 and docetaxel on MDA-MB-231 TNBC cells.
- To elucidate the underlying mechanisms of this combination therapy, focusing on apoptosis and reactive oxygen species (ROS) generation.
Main Methods:
- MDA-MB-231 cells were treated with varying concentrations of SBFI-26 and docetaxel, individually and in combination.
- Flow cytometry was used to assess cell cycle arrest and apoptosis.
- Western blotting analyzed apoptosis-related proteins (Caspase3, Bcl-2, Bax).
- Intracellular ROS levels were measured using a fluorescence spectrophotometer.
Main Results:
- The combination treatment significantly increased the proportion of G1 phase (apoptotic) cells and the overall apoptosis rate compared to individual treatments.
- Combination therapy led to decreased Bcl-2 expression and increased Bax and Caspase3 expression.
- SBFI-26 and docetaxel combination markedly elevated intracellular ROS levels in MDA-MB-231 cells.
Conclusions:
- Co-administration of SBFI-26 with docetaxel synergistically enhances apoptosis in triple-negative breast cancer cells.
- The combination therapy's efficacy is mediated, in part, by the elevation of intracellular ROS levels.
- This combination represents a potential therapeutic strategy for triple-negative breast cancer.
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