Arctigenin inhibits proliferation of ER-positive breast cancer cells through cell cycle arrest mediated by GSK3-dependent cyclin D1 degradation

To this end, the current study focuses on understanding the mechanism of Arc on ER-positive breast cancer cells. Main

Colony formation experiments and sulforhodamine B methods were used to determine the growth-inhibitory effect of Arc. The cell cycle and apoptosis were analyzed by flow cytometry. Alterations of signaling proteins were measured by Western blotting. Protein degradation was determined by comparing protein half-lives and inhibiting proteasome. Key findings: The experimental

These findings warrant the potential of Arc as a candidate treatment for ER-positive breast cancer.