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Name
Prof. Yi-Ching Wang (王憶卿 特聘教授)
Affiliations
Institute of Basic Medical Sciences & Department of Pharmacology, College of
Medicine, National Cheng Kung University, Tainan, Taiwan.(成大基礎醫學所＆藥理所)
TEL：06-2353535 ext.5502
E-mail: [email protected]
Biography
Dr. Yi-Ching Wang studies the molecular mechanisms involved in lung tumorigenesis. Dr. Wang
investigates the etiological association of alterations in tumor suppressor genes and oncogenes with
lung tumorigenesis. The alteration analyses include the following aspects: gene mutation and
polymorphism, gene loss, hypermethylation of promoter, chromatin structure alteration of gene
locus, mRNA alteration, and protein expression alteration. More recently, Dr. Wang has continued to
do research on cancer genomics and epigenomics such as genome-wide search of loss of
heterozygosity, and genome-scanning approaches of DNA methylation and chromatin alteration
profiles for identification of new genes critical to lung tumorigenesis. Several potential anti-cancer
drugs also are developing in her laboratory. Dr. Wang has published more than 80 SCI papers on
lung cancer including prestigious journals such as J Clin Oncol, J Clin Invest, Cancer Res, and Nat
Commun. Dr. Wang is one of the recipients of the Excellent Research Award of Taiwan Ministry of
Science and Technology.
Abstract
(1) The role of small GTPase Rab37 in regulation of exocytosis and cell motility
(2) Rab small GTPases are master regulators of membrane trafficking and guide vesicle targeting.
Recent publications show that Rab-controlled trafficking pathways are altered during
tumorigenesis. However, whether any of the Rabs plays a metastasis suppressor role is least
explored. Here, we address the metastasis suppressive function of human Rab37 (hRAB37)
using secretomics, cell, animal, and clinical analyses. We show that tissue inhibitor of
metalloproteinase 1 (TIMP1), a secreted glycoprotein that inhibits extracellular matrix turnover,
is a novel cargo of hRAB37. hRAB37 regulates the exocytosis of TIMP1 in a
nucleotide-dependent manner to inactivate matrix metalloproteinase 9 (MMP9) migration axis in
vitro and in vivo. Dysfunction of hRAB37 or TIMP1 abrogates metastasis suppression. Lung
cancer patients with metastasis and poor survival show low hRAB37 protein expression
coinciding with low TIMP1 in tumors. Our findings identify hRAB37 as a novel metastasis
suppressor Rab that functions through the TIMP1-MMP9 pathway and has significant prognostic
power. Additionally, the effectors in Rab37-mediated exocytosis and their role in cancer cell
motility control will be discussed in my speech.