Role of Metastasis Suppressor CD82 in the Deactivation of the C-Met Signaling Pathway in Prostate Cancer

Publication Year:
2017
Usage 8
Abstract Views 8
Repository URL:
https://scholarworks.gvsu.edu/gradshowcase/2017/cell_molecular_bio/2
Author(s):
Uhl, Katie L.; Sridhar, Suganthi
Tags:
Life Sciences
artifact description
PURPOSE: Prostate cancer is the second leading cause of cancer deaths among men in the United States. Metastasis plays a major role in patient prognosis and treatment options. One of the factors that has been proven to influence metastasis is the activation of the c-Met signaling pathway. Activation of the growth factor c-Met results in cytoskeletal rearrangement, migration and invasion. Previous studies have shown CD82 to act as an active metastatic suppressor in normal, healthy cells, and is downregulated in various forms of cancer. When CD82 is re-expressed in cancer cells, the cells no longer express metastatic characteristics. The purpose of this study was to determine what effect, if any, re-expression of CD82 in prostate cancer cells had on c-Met mediated migratory characteristics. METHODS AND MATERIALS: Two prostate cancer cell lines were utilized for this project. PC3-29 cells have been engineered with a vector that expresses CD82 and PC3-5V carry an empty vector and used as a control in this study. ANALYSES: Expression levels of CD82, c-Met, and related migratory proteins and activation state of c-Met were determined via western blot analysis. Visualization of cytoskeletal changes was done by immunostaining F-actin fibers and focal adhesions. RESULTS: Re-expression of CD82 in PC3-29 cells led to a decrease in c-Met activation. CD82 prevented the formation of F-actin fibers and focal adhesions needed for metastasis. CONCLUSIONS: CD82 directly impacts the activation levels of c-Met by preventing the phosphorylation of downstream effector molecules, halting the cytoskeletal changes needed for metastasis to occur.