Dr YAM Wai Ping, Judy | judyyam@pathology.hku.hk
Assistant Professor
BSc Washington; MSc HK; PhD HK
Molecular biology in human cancers
Research Description
My research interest focuses on the functional characterization of tumor suppressors and oncogenes and elucidation of cellular signaling pathways which contribute to the pathogenesis of cancers. My recent research has contributed to the better understanding of the functional roles and related signaling pathways of tumor suppressor, DLC1 (deleted in liver cancer 1). The tumor suppressor role and epigenetic regulation of DLC1 have been well studied in various cancers. To elucidate the underlying mechanism of the functional role of DLC1, our group has identified and characterized a focal adhesion protein, tensin2 as the first and novel interacting partner of DLC1. Our study has provided the first evidence of the subcellular localization of DLC1 in focal adhesions which is crucial for the tumor suppressive activities of DLC1.
Having demonstrated the tumor suppressor activities and epigenetic regulation of DLC1 in liver cancer in our previous studies, we are moving into the basic and mechanistic study of DLC1. Our current study on nucleocytoplasmic shuttling of DLC1 emphasizes the importance of subcellular localization in the biological roles of DLC1. Our study will address the mechanism and functional implications of nucleocytoplasmic shuttling of DLC1. Another focus of our group is delineating the upstream regulatory mechanism of DLC1. The mechanism underlying the regulation of DLC1 potentially has great impacts on the functions of DLC1.
Another area of our research team focuses on the study of focal adhesion proteins. Focal adhesions are structural links between extracellular matrix and actin cytoskeleton and are important sites of signal transduction. A number of diverse focal contact proteins are interconnected at the focal adhesions. Dysregulation of focal adhesion proteins has been implicated in various cancers and contributed to the acquired metastatic behavior of cancer cells. We are currently working on integrin-linked kinase and caveolin, two key adaptor proteins in focal adhesions. Functional characterization and investigation of the mechanistic basis of integrin-linked kinase and caveolin in the pathogenesis of liver cancer are undergoing.
Research Grants
RGC - General Research Fund (GRF)
- Interplay of caveolin-1 and Met receptor in liver cancer metastasis (2010)
- Nucleocytoplasmic shuttling mechanism of DLC1 tumor suppressor in liver cancer (2007)
- Characterization of tensin2, the binding partner of DLC1 tumor suppressor in liver cancer (2006)
Awards and Honors
- The University of Hong Kong Outstanding Young Researcher Award (2008-2009)
- Society of Chinese Bioscientists in America Travel award (2004)
Selected Publications
Click here for detail publication list on PubMed
Tse EYT, Ko FCF, Tung EKK, Chan LK, Lee TKW, Ngan ESW, Man K, Wong AST, Ng IOL, Yam JWP. 2011. Caveolin-1 is overexpressed and associated with hepatocellular carcinoma tumorigenesis and metastasis. J Pathol doi: 10.1002/path.3957.
Chan LK, Ko FCF, Sze KMF, Ng IOL, Yam JWP. 2011. Nuclear-targeted Deleted in Liver Cancer 1 (DLC1) is less efficient in exerting its tumor suppressive activity both in vitro and in vivo. PLoS ONE 6(9):e25547.
Chan J, Ko FCF, Ng IOL, Yam JWP. 2011. Integrin-linked kinase overexpression and its oncogenic role in promoting tumorigenicity of hepatocellular carcinoma. PLoS ONE 6(2):e16984.
Ko FCF, Chan LK, Tung EKK, Lowe SW, Ng IOL, Yam JWP. 2010. Akt phosphorylation of Deleted in Liver Cancer 1 deregulates its suppression of liver cancer tumorigenesis and metastasis. Gastroenterology 139(4):1397-1407.
Ko FCF, Yeung YS, Wong CM, Chan LK, Poon RTP, Ng IOL, Yam JWP. 2010. Deleted in liver cancer 1 isoforms are distinctly expressed in human tissues, functionally different and under differential transcriptional regulation. Liver International 30:139-148.
Yam JWP, Wong CM, Ng IOL. 2010. Molecular and functional genetics of hepatocellular carcinoma. Frontiers in Bioscience (Schol Ed) 2:117-134. (Review)
Chan LK, Ko FCF, Ng IOL, Yam JWP. 2009. Deleted in liver cancer 1 (DLC1) utilizes a novel binding site for tensin2 PTB domain interaction and is required for tumor suppressive function. PLoS ONE 4(5):e5572.
Yam JWP, Tse EYT, Ng IOL. 2009. Role and significance of focal adhesion proteins in hepatocellular carcinoma. J Gastroenterol Hepatol 24:520-530. (Review)
Yam JWP, Ko FCF, Chan CY, Yau TO, Tung EKK, Leung THY, Jin DY, Ng IOL. 2006. Tensin2 variant 3 is associated with aggressive tumor behavior in human hepatocellular carcinoma. Hepatology 44:881-890.
Yam JWP, Ko FCF, Chan CY, Jin DY, Ng IOL. 2006. Interaction of DLC1-tensin2 complex with caveolin-1 and implications in tumor suppression. Cancer Research 66:8367-8372.
Wong CM*, Yam JWP*, Ching YP, Yau TO, Leung HY, Jin DY, Ng IOL. 2005. Rho GTPase activating protein DLC1 (deleted in liver cancer 1) suppresses cell proliferation and invasion in hepatocellular carcinoma. Cancer Research 65:8861-8868. *Both contributed equally
Yam JWP, Chan KW, Ngan ESW, Hsiao WLW. 2005. Genomic structure, alternative splicing and tissue expression of rFrp/sFRP-4, the rat frizzled related protein gene. Gene 357:55-62.
Yam JWP, Jin DY, So CW, Chan LC. 2004. Identification and characterization of EBP, a novel EEN binding protein that inhibits ras signaling and is recruited into the nucleus by the MLL-EEN fusion protein. Blood 103:1445-1453.
Yam JWP, Chan KW, Hsiao WLW. 2003. Transcriptional regulation of rat frizzled related protein gene promoter by CREB. Oncogene 22:3901-3910.
Yam JWP, Chan KW, Hsiao WLW. 2001. Suppression of the tumorigenicity of mutant p53-transformed rat embryo fibroblasts through expression of a newly cloned rat nonmuscle myosin heavy chain-B. Oncogene 20:58-68.