Rong Li, Ph.D.

Professor

Profile and Contact Information | Research | Laboratory

RESEARCH

Our laboratory addresses the following three fundamental questions concerning breast cancer treatment and prevention.

1. How does BRCA1 suppress tumor development in a gender- and tissue-specific manner? Women who carry cancer-predisposing germ-line mutations in BRCA1 have significantly increased chance of developing breast and ovarian cancers. While the BRCA1 activity in DNA repair is clearly important to the etiology of BRCA1-associated cancers, it is not clear whether the DNA repair function alone is sufficient to account for the gender- and tissue-specific tumor suppression by BRCA1. We previously identified a BRCA1-binding protein COBRA1, which is identical to the B subunit of NELF involved in pausing of RNA polymerase II. Using mouse genetics and clinical samples from BRCA1 mutation carriers, we are investigating whether a crosstalk between BRCA1 and COBRA1-regulated transcription machinery contributes to the tissue-specific function of BRCA1 in breast epithelium.

2. How can the antitumor activity of estrogen receptor (ER) be mobilized?In contrast to the tumor-promoting activity of ER, ER inhibits tumor growth in breast cancer. Because ER is present in a significant percentage of breast cancer cases, rallying its antitumor activity could serve as a potential therapeutic approach. Our pioneer discovery of a phosphotyrosine switch for the antitumor activity of ER enables us to mobilize ER function with unprecedented precision. We are testing the hypothesis that turning on this molecular switch of ER can inhibit triple negative breast cancer and circumvent hormonal resistance of ER-positive breast cancer, two clinically pressing areas where therapeutic potential of ER has been previously demonstrated.

3. How do adipose stromal cells (ASC) promote breast cancer progression?ASC is a major constituent of the breast and a source of tumor-promoting factors including estrogens. We recently discovered a new mechano-transducing pathway that links mechanical phenotype with the endocrine/paracrine output of ASCs. This pathway is initiated by a cell surface receptor called discoidin domain receptor 1 (DDR1). Combining three-dimension cell culture systems and animal models, we are exploring novel therapeutic approaches to disrupt this stroma-tumor communication.

Selected Publications

Complete list of published work.

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Faculty Research - Department of Molecular Medicine ...