Fang-Tsyr Lin, MD, PhD
Baylor College of Medicine
RIP6 Regulates p27KIP1 to Promote Ovarian Tumorigenesis
The CDK inhibitor p27KIP1 is traditionally viewed as a tumor suppressor by inhibiting cell cycle progression. However, the cytosolic mislocalized p27KIP1 can induce ovarian cancer cell invasion. Dr. Lin has shown that these opposing effects are regulated through the interaction of p27KIP1 with the adaptor protein TRIP6, which is expressed at high levels in ovarian cancers. TRIP6 cooperates with AKT to promote the oncogenic effect of cytosolic p27KIP1 but regulates growth factor-induced nuclear p27KIP1 degradation to promote cancer cell proliferation. This project aims to elucidate the novel mechanisms and consequences of these regulations to find better strategies for ovarian cancer therapy.