Takaku named Project Leader on NIH Breast Cancer Grant

Motoki Takaku, Ph.D. will assume the role of Project Leader on a on year NIH grant titled, "Mechanism of Tumor Suppressor Function of Progesterone Receptor in Breast Cancer." This project is a supplemental award to the Epigenetics and Epigenomics Center of Biomedical Research Excellence (CoBRE), on which Biomedical Sciences' Dr. Roxanne Vaughn is primary investigator.

Dr. Takaku said, "In short, the main goal is to identify how progesterone receptor (PR) controls breast cancer cell proliferation. We believe the identification of such mechanisms will contribute to the development of novel therapeutic strategies for aggressive breast cancer."

Breast cancer is the second common cancer among women in the US. In 2020, about 276,000 new cases of invasive breast cancer are expected to be diagnosed, and approximately 42,000 women in the U.S. are expected to die from breast cancer. Steroid hormones and hormone receptors are known to be key factors of the breast cancer risk. Long-term exposure to progesterone or progestin (synthetic version of progesterone) is known to be associated with higher risk of breast cancer, ovarian cancer, and other diseases. On the other hand, other studies also suggest that short-term progesterone exposure can inhibit breast tumor growth and risk. Although progesterone treatment has been considered as a promising breast cancer treatment, the clinical significance of progesterone treatment is still obscure because of this controversial function of progesterone in breast cancer and our lacking knowledge of the molecular mechanism of progesterone receptor (PR) action in breast cancer. This application aims to fill this critical gap and tries to contribute to the development of progesterone targeting therapeutic strategies by using our unique breast cancer cell model as well as cutting edge genomics approaches, which have been significantly developed through the parent CoBRE program. The goal of this project is to identify how PR regulates cell cycle genes to inhibit tumor growth.