Abstract

CD82 (KAI), a metastasis tumor suppressor protein is under-expressed in prostate as well as several other types of metastatic cancers. It inhibits cancer metastasis, but the mechanism through which regulation happens remains unclear. Various pathways are being explored in this lab, including regulation of c-MET, a growth factor receptor observed to have increased activation in tumor cells. CD82 and c-MET do not co-localize, suggesting that CD82 indirectly downregulates c-MET. To be expressed, c-MET first needs to bind to its ligand, HGF. This growth factor encourages phosphorylation of c-MET, consequently activating it. C-Met has four tyrosine phosphorylation sites that include p-Tyr 1003, p-Tyr 1234/1235, p-Tyr 1349 and p-Tyr 1365. Knowing how each phosphorylation site of c-Met affects downstream signaling event, our lab is focused in identifying which site is regulated by CD82. This will provide further insight into how CD82 regulates c-Met and prevents prostate tumor metastasis and help develop drugs that can target these molecules.