Professor, Department of Pharmacology
University of South Florida, USA
"Dr. Hong-Gang Wang is the Lois High Berstler Professor in the Department of Pharmacology and the Penn State Hershey Cancer Institute at the Penn State University College of Medicine. He earned his PhD from the University of Tsukuba in Japan in 1992, and conducted his postdoctoral research in apoptosis with Dr. John Reed at the Burnham Institute for Medical Research from 1993 to 1998. He joined the Drug Discovery Program at the H. Lee Moffitt Cancer Center& Research Institute as an Assistant Professor in 1998, advancing to the rank of Professor, before moving to the Penn State Hershey Medical Center in 2008. Research in the laboratory of Dr. Wang is concerned with understanding of the fundamental mechanisms that control apoptosis and autophagy in the context of oncogenesis. Drug discovery through the development of small molecules that directly target the molecular components of apoptosis and autophagy is another of the major research interests of Dr. Wang and his laboratory co-workers. Dr. Wang is considered an expert in this area of research. He is frequently asked to review manuscripts for numerous journals and to serve on government and foundation study sections. He serves on the Editorial Advisory Panel for the Biochemical Journal and theEditorial Board for The WJBCand is a permanent member of the Cancer Molecular Pathobiology Study Section of the National Institutes of Health.Dr. Wang has received numerous grants for his research from government and private funding agencies and has been continuously funded since 1998. His work has resulted in the publication of over 100 research articles. "
Research in my laboratory is concerned with understanding the fundamental mechanisms that control apoptosis and autophagy in the context of oncogenesis. Drug discovery through the development of small molecules that directly target the molecular components of apoptosis and autophagy is another major interest of our research. Apoptosis (self-killing) is the most well defined form of physiological cell death and has long been used as a synonym for programmed cell death. In contrast, autophagy (self-eating) is a lysosomal degradation pathway and is generally thought to be a cytoprotective mechanism. However, recent observations have also indicated that autophagy may contribute to cell death under certain circumstances. Although extensive crosstalk clearly exists between apoptosis and autophagy, the regulators that govern this crosstalk remain far from clear.Our recent studies suggest that the formation of an intracellular death-inducing signaling complex (iDISC) on the autophagosomal membrane is able to switch autophagy from pro-survival to pro-apoptotic signaling. Moreover, my laboratory has cloned and characterized a member of the endophilin family Bif-1, also known as endophilin B1 or SH3GLB1, as a novel Bax activator and autophagy modulator. We have demonstrated that the loss of Bif-1 not only suppressesBax-mediated mitochondrial apoptosis but also impairs autophagy.Bif-1 interacts with Beclin1 through UVRAG and regulates autophagosome formation and Atg9 trafficking possibly through the mediation of Golgi fragmentation. Importantly, the expression of Bif-1 is lost or decreased in various human cancers, and the deletion of Bif-1 promotes tumor development in mouse models. Currently, we are exploring the precise mechanisms underlying Bif-1-mediated apoptosis and autophagy to better understand how Bif-1 functions as a tumor suppressor. In addition, our group has been collaborating with medicinal chemists during the past decade for the development and characterization of novel anticancer agents such as Bcl-2 specific inhibitors.The ultimate goal of my laboratory is to translate basic science research discoveries to the development of new approaches for the prevention and treatment of cancer.