Daiqing Liao, Ph.D., an associate professor in the department of anatomy and cell biology in the University of Florida College of Medicine, has been awarded a $569,400 grant from the Florida Department of Health James and Esther King Biomedical Research Program to define the molecular mechanism and signaling pathways that promote DAXX-mediated lipid synthesis and resistance to ferroptosis in triple negative breast cancer models.
Triple negative breast cancer is a subtype of breast cancer that lacks expression of estrogen receptors, progesterone receptors and HER2, making it more difficult to treat. Triple negative breast cancer is also more resistant to chemotherapy and radiation, making it important to identify new therapeutic targets. DAXX, a protein that regulates cell death and survival, has been shown to promote the growth of triple negative breast cancer cells and resistance to ferroptosis, a form of cell death triggered by damaged phospholipids in cell membranes. Despite previous research, the molecular mechanisms and signaling pathways behind these effects are not fully understood.
The Liao lab aims to use molecular, cellular and bioinformatics approaches and animal models to clarify the mechanism by which DAXX controls lipid synthesis and prevents ferroptosis under the regulation of RAS and mTORC1 signaling.
“We are excited to define the molecular mechanism and signaling pathways that promote DAXX-mediated lipid synthesis and resistance to ferroptosis in triple negative breast cancer models,” said Liao, who is a member of the Cancer Center’s Mechanisms of Oncogenesis research program. “Triple negative breast cancer is a challenging subtype of breast cancer to treat, and identifying new therapeutic targets is crucial for improving patient outcomes.”
This grant will allow Liao and the team to make strides in understanding the role of DAXX in triple negative breast cancer and the potential for targeting it as a therapeutic option. The funding will allow the team to define the molecular mechanisms and signaling pathways that mediate the effects of DAXX on triple negative breast cancer. Once defined, these pathways can be evaluated as a therapeutic approach. Liao and his team aim to determine the potential effectiveness and safety of these therapies.