The Effect of RYBP Expression on the Invasion and Migration of Glioblastoma Cells
Poster Number
1
Session Title
Poster Session 1
Faculty Mentor
Daniel Stovall, Ph.D., Laura Glasscock, Ph.D., and Kathryn Kohl, Ph.D.
College
College of Arts and Sciences
Department
Biology
Abstract
Glioblastoma multiforme (GBM) is the most aggressive and invasive form of cancer in the central nervous system. It arises from astrocytes, a type of star-shaped glial cell that support the nerve impulse-conducting neurons of the nervous system. GBM tumors are diffuse, with tendril-like processes that extend from the tumor into surrounding healthy tissue. This, along with limited efficacy of available treatment modalities, contributes to the abysmal survival rates among GBM patients. Previous research has determined that RING1- and YY1-binding protein (RYBP), a chromatin-modifying Polycomb protein, is downregulated in nearly 50% of GBM patient tumors compared to adjacent normal brain tissue. Therefore, RYBP may act as a tumor suppressor gene in GBM. Indeed, RYBP’s tumor suppressive effects have been reported in various solid tumors. To investigate the tumor suppressive role of RYBP in GBM cells, we transiently induced RYBP expression in two glioma cell lines, U-87 and U-118, using a plasmid encoding RYBP or an empty control vector. Twenty-four hours after transfection, wound healing assays were performed to measure differences in cell migration, and Boyden chamber assays were performed to measure differences in cell invasion. RYBP expression in transfected cells was also confirmed by Western blot. RYBP expression significantly reduced GBM migration and invasion in U-118 cells, and non-significantly decreased these phenotypes in U-87 cells. Because the rapid invasion of GBM tumors into healthy brain tissue is a major contributor to patient mortality, revealing genes that contribute to GBM cell invasion may contribute to development of new targeted, more effective therapies.
Honors Thesis Committee
Daniel Stovall, Ph.D., Laura Glasscock, Ph.D., and Kathryn Kohl, Ph.D.
Previously Presented/Performed?
Winthrop University Showcase of Winthrop University Undergraduate Research and Creative Endeavors, Rock Hill, SC, April 2022 and 2023
Type of Presentation
Poster presentation
Grant Support?
Supported by SC-INBRE DRP 5P20GM103499-21
Start Date
15-4-2023 12:00 PM
The Effect of RYBP Expression on the Invasion and Migration of Glioblastoma Cells
Glioblastoma multiforme (GBM) is the most aggressive and invasive form of cancer in the central nervous system. It arises from astrocytes, a type of star-shaped glial cell that support the nerve impulse-conducting neurons of the nervous system. GBM tumors are diffuse, with tendril-like processes that extend from the tumor into surrounding healthy tissue. This, along with limited efficacy of available treatment modalities, contributes to the abysmal survival rates among GBM patients. Previous research has determined that RING1- and YY1-binding protein (RYBP), a chromatin-modifying Polycomb protein, is downregulated in nearly 50% of GBM patient tumors compared to adjacent normal brain tissue. Therefore, RYBP may act as a tumor suppressor gene in GBM. Indeed, RYBP’s tumor suppressive effects have been reported in various solid tumors. To investigate the tumor suppressive role of RYBP in GBM cells, we transiently induced RYBP expression in two glioma cell lines, U-87 and U-118, using a plasmid encoding RYBP or an empty control vector. Twenty-four hours after transfection, wound healing assays were performed to measure differences in cell migration, and Boyden chamber assays were performed to measure differences in cell invasion. RYBP expression in transfected cells was also confirmed by Western blot. RYBP expression significantly reduced GBM migration and invasion in U-118 cells, and non-significantly decreased these phenotypes in U-87 cells. Because the rapid invasion of GBM tumors into healthy brain tissue is a major contributor to patient mortality, revealing genes that contribute to GBM cell invasion may contribute to development of new targeted, more effective therapies.
