Chune Dong

1. Introduction Estrogen receptors (ER), encompassing ERα and ERβ, are pivotal in orchestrating target gene expression through signal transduction and transcription factors [1]. ERα, particularly overexpressed in ER-positive (ER+) breast cancer (BC), stands as a crucial driver in the formation and progression of ER+ BC, making it a prime therapeutic target [2]. Endocrine therapy, a cornerstone in ER+ BC treatment, operates by inhibiting estrogen biosynthesis and its interaction with ER [3,4].