Date of Award

8-2016

Degree Type

Thesis

Degree Name

Master of Science

Department

Biology

Program

Biology

First Advisor/Chairperson

Robert Belton, Jr., Ph.D.

Second Advisor

Robert Winn, Ph.D.

Third Advisor

John Lawrence, Ph.D.

Abstract

Glioblastoma (GBM) is one of the most aggressive forms of brain tumor. With the current standard of care, survival prognosis for GBM patients is 15 months with a five-year survival rate of less than 3%. An increased understanding of the molecular mechanisms leading to cell growth and survival of GBMs may result in novel treatments to target and eradicate the disease. The protein Basigin-2 (aka EMMPRIN) induces the expression of matrix metalloproteinase (MMP) enzymes, and its expression level is positively correlated with GBM tumor grade. In 2011, Liao et al. reported that a splice variant of the basigin gene, called Basigin-3, may have an inhibitory function when bound to Basigin-2 in Human Hepatocellular Carcinoma (HHC) cells, as it decreases tumor growth, invasion and MMP expression. The goal of this study is to determine the effects of Basigin-3 overexpression in GBM cell growth. For this a recombinant fusion protein consisting of Basigin-3 and the red fluorescent protein mKate2 was overexpressed in a GBM cell line (LN229). RT-PCR and RT-qPCR was used to measure MMP gene expression in Basigin-3/mKate2 expressing cells, and confocal microscopy used to confirm over-expression of Basigin-3 in the transfected populations. Our hypothesis that Basigin-3 overexpression would reduce MMP expression cells was not supported by our data suggesting that Basigin-3 in GBM does not as an inhibitor of Basigin-2 function in GBM cells.

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