Wanjin Hong
Wanjin HONG graduated from Xiamen University (Fujian, China) in 1982 and was one of a few hundred Chinese students chosen for further graduate training in the United States via the CUSBEA program. He received his PhD from the State University of New York (SUNY Buffalo), and was a postdoctoral fellow there before he joined the Institute of Molecular and Cell Biology (IMCB) in Singapore as a principal investigator in 1989. He was the recipient of National Science Award in 1999 in Singapore. Presently, he is a Professor and Executive Director of IMCB. He serves as the Editor-in-Chief of Bioscience Reports and is on the editorial board of TRAFFIC.
Prof Hong has also made significant contributions in the field of cancer cell biology. His early works demonstrated that E2F1 is sufficient to confer oncogenic growth. He has identified human Hbrm as a novel interacting protein of the tumor suppressor retinoblastoma protein. His recent work has demonstrated that TAZ is a novel oncogene and is able to promote cell migration, invasion and tumorigenesis. Prof Hong’s future studies will focus on the physiological role of two SNAREs (VAMP8 and VAMP5), three PX-domain sorting nexins (SNX3, SNX12 and SNX27) and two small GTPases (Rab34 and Rab36) by analyzing the knockout mice. The mechanism governing the role of TAZ/YAP in promoting invasiveness of breast cancer or other cancers will be studied by focusing on interacting proteins and downstream target genes.
Prof Hong has also made significant contributions in the field of cancer cell biology. His early works demonstrated that E2F1 is sufficient to confer oncogenic growth. He has identified human Hbrm as a novel interacting protein of the tumor suppressor retinoblastoma protein. His recent work has demonstrated that TAZ is a novel oncogene and is able to promote cell migration, invasion and tumorigenesis. Prof Hong’s future studies will focus on the physiological role of two SNAREs (VAMP8 and VAMP5), three PX-domain sorting nexins (SNX3, SNX12 and SNX27) and two small GTPases (Rab34 and Rab36) by analyzing the knockout mice. The mechanism governing the role of TAZ/YAP in promoting invasiveness of breast cancer or other cancers will be studied by focusing on interacting proteins and downstream target genes.