Combining Chemotherapy Agents and Autophagy Modulators for Enhanced Breast Cancer Cell Death
This study highlights the impact of combined arsenic trioxide (ATO), carboplatin (CP), and cyclophosphamide (CY) on triple-negative breast cancer (TNBC) cell lines, specifically BT-20 and MDA-MB-231. Given TNBC’s aggressive nature and limited targeted treatment options, investigating autophagy modulation and apoptosis induction presents a promising therapeutic avenue.
The experimental methods employed included MTT assays to determine cytotoxicity, flow cytometry for apoptosis and cell cycle progression analysis, and RT-PCR to quantify gene expression of key markers such as Beclin 1, LC3, caspase-3, and BCL2. Statistical analysis via one-way ANOVA followed by Dunnett’s test ensured robust validation of findings.
Results indicated a significant reduction in cell viability upon combination treatment, along with increased caspase-3 activity and decreased BCL2 expression, demonstrating enhanced apoptosis. Further, the study identified G1 phase cell cycle arrest and upregulated autophagy markers Beclin 1 and LC3, signifying potential interplay between autophagy and apoptosis.
These findings suggest that the synergistic action of ATO, CP, and CY may provide an effective strategy for TNBC treatment GDC-0980, potentially improving therapeutic outcomes for patients with resistant disease. Future studies could further explore mechanistic pathways, in vivo validation, and clinical translational potential to optimize dosing and minimize toxicity.