Sennoside B inhibits malignant phenotypes of triple-negative breast cancer cells and represses ERK/AKT/STAT5 signaling

Triple-negative breast Cancer (TNBC) is the most lethal subtype of breast Cancer. Treatment alternatives for TNBC are very limited and new therapeutic drugs are needed. Sennoside B (SB) is a dianthrone glycoside that has shown antitumor activity in osteosarcoma. However, the role of SB in TNBC remains unclear. This study aims to investigate the role and potential mechanism of SB in TNBC. MTT, colony formation, scratch, and Transwell assays were conducted to examine the malignant behaviors of TNBC cells under different doses of SB treatment. RT-qPCR and western blotting were utilized to detect mRNA or protein levels of molecules. The results revealed that SB treatment dose-dependently restrained TNBC cell proliferation, migration, invasiveness as well as epithelial-mesenchymal transition. Mechanistically, SB suppressed extracellular signal-regulated kinase (ERK), Ak strain transforming protein (Akt), and signal transducer and activator of transcription 5 (STAT5) phosphorylation in TNBC cells. In conclusion, SB treatment impairs the cell aggressiveness of TNBC and blocks ERK/Akt/STAT5 signaling in TNBC cells.

Invasion; Proliferation; Sennoside B; Signaling pathway; TNBC.