Developmental and Cell Biology and Biological Chemistry
University of California
BRCA1 is involved in many cellular activities including DNA repair, cell cycle checkpoints and gene expression regulation, largely through forming different protein complexes. Recent studies indicate that BRCA1-deficient breast tumor cells harbor alterations in metabolism, as do other cell types in the tumor environment of BRCA1-deficient tumors. These changes generate a specific microenvironment to promote cancer growth. In earlier work, Dr. Lee and her team performed studies to identify genome-wide bindings of BRCA1 and its interacting partner, ZBRK1, and found that the process of steroid biosynthesis is regulated by the BRCA1-ZBRK1 complex. In the coming year they will study whether this pathway is important for growth of BRCA1-deficient mammary epithelial cells and whether inhibitors of this pathway would be effective in the prevention of BRCA1-associated tumor growth.
Eva YHP Lee is the Chancellor’s Professor in the Department of Biological Chemistry at the University of California, Irvine School of Medicine.
In the late 1980’s, Dr. Lee reported the inactivation of the prototypic tumor suppressor gene, the retinoblastoma susceptibility gene (RB), in breast cancer. Subsequently, she and her team investigate how cells repair DNA breaks and identified new players that slow down the cell cycle while DNA damages are being repaired.
Her laboratory has established several breast cancer models to address the breast-specific function of the breast cancer susceptibility gene, BRCA1. They found that BRCA1 plays a role regulating the levels of progesterone receptors (PR). Her team has investigated the mechanisms involved and addressed whether anti-progesterone could be used to delay mammary tumors using the model systems. In addition, Dr. Lee and her team are exploring the link between the circadian system, BRCA1 and the regulation of female hormones.