Breviscapine Induces Breast Cancer Cell Cycle Arrest and Apoptosis by Modulating the Jak-Stat Pathway

The aim of this study was to investigate the effects and possible mechanisms of breviscapine arrest in the development of breast cancer cells. Cell viability, cycle arrest, and apoptosis were measured using 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazoliumbromide assay and flow cytometry in MCF-7 cells treated with increasing concentrations of breviscapine. In addition, the expression level of cyclin D1, p21, cleaved caspase-3, and poly ADP-ribose polymerase, p-Janus kinase 2 and p-signal transducers and activators of transcription 3 was analyzed using western blot assay. The results showed that breviscapine suppressed cell viability and induced apoptosis in MCF-7 cells in a dose-dependent fashion. Breviscapine also increased MCF-7 cell number in the G1 phase and decreased that in the S phase. Moreover, cyclin D1, p-JAK2/JAK2, and p-STAT3/STAT3 expression levels were down-regulated, while p21, cleaved caspase-3, and poly ADP-ribose polymerase expression levels were up-regulated in breviscapine-treated MCF-7 cells. In conclusion, breviscapine regulates breast cancer viability, cell cycle arrest, and apoptosis in a concentration-dependent manner by modulating the JAK-STAT pathway.