Title of Abstract

Using RYBP Expression to Suppress GBM Cell Viability

Poster Number

66

Submitting Student(s)

Daniela Torricos

Faculty Sponsor (for work done with a non-Winthrop mentor)

Daniel Stovall, Ph.D.

College

College of Arts and Sciences

Department

Biology

Abstract

Glioblastoma multiforme (GBM) is an aggressive and rare type of malignant tumor of the brain and has a survival rate of 22% in younger patients and 6% in older patients, once diagnosed. While these tumors can affect younger patients, it is more common for them to occur in patients ages 45 to 70. GBMs arise from astrocytes, a type of glial cell that supports neurons and participates in forming the the blood-brain barrier. Glioblastomas are particularly difficult to treat due to the formation of microscopic outgrowths that burrow deep into nearby healthy tissue. Due to these outgrowths, regular cancer treatments like chemotherapy, radiation therapy, and surgery are not very effective ways to actively treat GBM. Thus, we sought to investigate epigenetic networks that mediate GBM progression. We measured the difference in cell viability resulting from forced RYBP expression. RYBP is a Polycomb group protein necessary for transcriptional repression and regulation of cell growth. We transfected U-87 and U-118 GBM cell lines with an RYBP expressing plasmid and measured differences in cell viability and apoptosis, or cell death, compared to control cells that were transfected with an empty vector. RYBP expression was confirmed by Western blot. Cell viability was measured with a Trypan blue exclusion assay and the activation of apoptosis was detected by measuring the levels of cleaved caspases in transfected U-87 and U-118 cells.

Start Date

15-4-2022 12:00 PM

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Apr 15th, 12:00 PM

Using RYBP Expression to Suppress GBM Cell Viability

Glioblastoma multiforme (GBM) is an aggressive and rare type of malignant tumor of the brain and has a survival rate of 22% in younger patients and 6% in older patients, once diagnosed. While these tumors can affect younger patients, it is more common for them to occur in patients ages 45 to 70. GBMs arise from astrocytes, a type of glial cell that supports neurons and participates in forming the the blood-brain barrier. Glioblastomas are particularly difficult to treat due to the formation of microscopic outgrowths that burrow deep into nearby healthy tissue. Due to these outgrowths, regular cancer treatments like chemotherapy, radiation therapy, and surgery are not very effective ways to actively treat GBM. Thus, we sought to investigate epigenetic networks that mediate GBM progression. We measured the difference in cell viability resulting from forced RYBP expression. RYBP is a Polycomb group protein necessary for transcriptional repression and regulation of cell growth. We transfected U-87 and U-118 GBM cell lines with an RYBP expressing plasmid and measured differences in cell viability and apoptosis, or cell death, compared to control cells that were transfected with an empty vector. RYBP expression was confirmed by Western blot. Cell viability was measured with a Trypan blue exclusion assay and the activation of apoptosis was detected by measuring the levels of cleaved caspases in transfected U-87 and U-118 cells.