Event Title

Identifying a Regulatory Role for the Tumor Metastasis Suppressor Gene KAI1/CD82 in Metastatic Prostate Cancer Cell Lines

Presentation Type

Poster/Portfolio

Presenter Major(s)

Cell and Molecular Biology

Mentor Information

Suganthi Sridhar

Department

Biomedical Sciences

Location

Henry Hall Atrium 63

Start Date

10-4-2013 9:00 AM

End Date

10-4-2013 10:00 AM

Keywords

Life Science

Abstract

KAI1/CD82, a metastasis prostate tumor suppressor gene has been shown to be down-regulated not only in prostate but also many other metastatic cancers. CD82 interacts with proteins and may act as a master regulator of membrane organization at the cell surface but the significance of these associations and CD82's role in metastasis prevention is unclear. By reintroducing CD82 into prostate tumor cells, we have shown CD82 to regulate c-Met activation and focused on identifying the downstream signaling molecules involved. In addition to c-Met we have reason to believe that there may be more proteins regulated by CD82. Microarray studies done on CD82 (+/-), on both tumor and normal prostate cells have identified genes involved in cell cycle, growth, and metastatic suppression being regulated and are currently under investigation. Identifying the proteins regulated by CD82 and deciphering the downstream signaling mechanisms involved in this regulation is the focus of our future studies.

This document is currently not available here.

Share

COinS
 
Apr 10th, 9:00 AM Apr 10th, 10:00 AM

Identifying a Regulatory Role for the Tumor Metastasis Suppressor Gene KAI1/CD82 in Metastatic Prostate Cancer Cell Lines

Henry Hall Atrium 63

KAI1/CD82, a metastasis prostate tumor suppressor gene has been shown to be down-regulated not only in prostate but also many other metastatic cancers. CD82 interacts with proteins and may act as a master regulator of membrane organization at the cell surface but the significance of these associations and CD82's role in metastasis prevention is unclear. By reintroducing CD82 into prostate tumor cells, we have shown CD82 to regulate c-Met activation and focused on identifying the downstream signaling molecules involved. In addition to c-Met we have reason to believe that there may be more proteins regulated by CD82. Microarray studies done on CD82 (+/-), on both tumor and normal prostate cells have identified genes involved in cell cycle, growth, and metastatic suppression being regulated and are currently under investigation. Identifying the proteins regulated by CD82 and deciphering the downstream signaling mechanisms involved in this regulation is the focus of our future studies.