Professor David Huang from WEHI visits IBP
On 21th May 2015, David Huang, Professor of Walter and Eliza Hall Institute of Medical Research visited IBP and gave a lecture entitled “Targeting Protein-Protein Interactions to Treat Cancers”.
Professor David Huang engaged in researches on the mechanism of apoptosis for many years, and tried to apply the bench results to clinical treatment. He has made great achievements in the study of Bcl-2 family regulated apoptosis, which has been used for the cancer treatment.
During his lecture, Professor David Huang gave a brief introduction of the mechanism of Bcl-2 family regulated apoptosis, the interactions between BH3-only protein and Bcl-2 family, and the design of antineoplastic drugs based on structural information. Bcl-2 family, including Bcl-2, Bcl-w, Bcl-xL and Mcl-1, is a kind of important apoptosis regulator proteins. It helps cell to survive by suppressing the release of cytochrome c through inhibiting Bax/Bak. As a result, they are also called as pro-survival proteins. Overexpression of Bcl-2 has been detected in vary kinds of cancer cells, indicating Bcl-2 a probable drug target. BH3-only proteins, for instance Bim and Bad, are the activators of apoptosis and named as pro-apoptotic proteins. They can activate apoptosis by either directly interact with Bax/Bak or block the function of Bcl-2 by interacting with the hydrophobic groove on the surface of Bcl-2. BH3-only proteins have selective binding activity and variable binding affinity with different members of Bcl-2 family. Professor Huang’s lab did a systematic research on the interactions between the pro-survival and pro-apoptotic proteins, and made a great contribution to this field. Based on their studies, researchers have designed a series of BH3-only mimics for treating cancers. ABT-737, a mimic of Bad, known as an inhibitor of Bcl-2, Bcl-xL and Bcl-w, is a successful example. It is now used in the treatment of several kinds of leukemia.
Professor David Huang’s lecture is inspiring and very impressive for all the audience.