Presentation (Project) Title

CD82 Regulation of c-Met in Metastatic Prostate Cell Lines

Mentor Information

Suganthi Sridhar (Department of Integrative Biology)

Presentation Format

Event

Abstract

CD82 (KAI1), a tetraspanin was first identified as a metastasis tumor suppressor in prostate cells. CD82 is downregulated not only in prostate cancer but also in a variety of many invasive epithelial tumors. CD82 has been well documented as an inhibitor of cell motility and invasion in cancer cells, with varied inhibitory mechanisms. By introducing CD82 in metastatic cell lines (PC3) that do not express CD82, we have shown CD82 to regulate c-Met, a growth factor receptor, over expressed and/or over activated in prostate tumors. Overactivation of c-Met promotes cell proliferation, migration and invasion and it is unclear how CD82 regulates c-Met. Using metastatic prostate cell lines (PC3), with and without CD82 we are using immuno-fluorescence , immunoprecipitation, flow cytometry and western blot techniques to analyze the exact mechanism by which CD82 regulates c-Met. Preliminary data indicates CD82 does not colocalize with CD82, nor does it downregulate c-Met expression on the cell surface. However, CD82 expression seems to cause varied distribution of c-Met and is currently being investigated. Preliminary indications are that CD151, another tetraspanin and a known tumor promoter may be involved in this regulation. CD151 associates with c-Met and our lab is currently exploring the redistribution pattern of CD151 as an alternate mechanism by which c-Met may be regulated . The results observed will provide insights into the role CD82 plays in c-Met regulation as well as it may overall play in CD151 redistribution and in tumor progression and metastasis in prostate cancer.

Streaming Media

This document is currently not available here.

Share

COinS
 

CD82 Regulation of c-Met in Metastatic Prostate Cell Lines

CD82 (KAI1), a tetraspanin was first identified as a metastasis tumor suppressor in prostate cells. CD82 is downregulated not only in prostate cancer but also in a variety of many invasive epithelial tumors. CD82 has been well documented as an inhibitor of cell motility and invasion in cancer cells, with varied inhibitory mechanisms. By introducing CD82 in metastatic cell lines (PC3) that do not express CD82, we have shown CD82 to regulate c-Met, a growth factor receptor, over expressed and/or over activated in prostate tumors. Overactivation of c-Met promotes cell proliferation, migration and invasion and it is unclear how CD82 regulates c-Met. Using metastatic prostate cell lines (PC3), with and without CD82 we are using immuno-fluorescence , immunoprecipitation, flow cytometry and western blot techniques to analyze the exact mechanism by which CD82 regulates c-Met. Preliminary data indicates CD82 does not colocalize with CD82, nor does it downregulate c-Met expression on the cell surface. However, CD82 expression seems to cause varied distribution of c-Met and is currently being investigated. Preliminary indications are that CD151, another tetraspanin and a known tumor promoter may be involved in this regulation. CD151 associates with c-Met and our lab is currently exploring the redistribution pattern of CD151 as an alternate mechanism by which c-Met may be regulated . The results observed will provide insights into the role CD82 plays in c-Met regulation as well as it may overall play in CD151 redistribution and in tumor progression and metastasis in prostate cancer.