{"id":{"repo_id":"nmu","oai_identifier":"oai:commons.nmu.edu:theses-1125"},"canonical_url":"https://search.dev.ndltd.org/etd/nmu/oai:commons.nmu.edu:theses-1125","repository":{"repo_id":"nmu","name":"Northern Michigan University","base_url":"https://commons.nmu.edu/do/oai/"},"display":{"title":"The Overexpression of Basigin-3 in Glioblastoma","abstract":"<p>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. </p>","abstract_html":"&lt;p&gt;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. &lt;/p&gt;","abstract_has_math":false,"creators":["Wightman, Samantha M"],"institution":null,"degree_name":"Master of Science","degree_level":"Thesis","degree_discipline":"Biology","degree_department":null,"school":null,"contributors":["Robert Belton, Jr., Ph.D."],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2016,"date_issued":"2016-08-01T07:00:00Z","date_published":"2016-08-01T07:00:00Z","updated_at":"2026-07-24T03:23:47Z","subjects":["GBM","basigin","BSG","glioblastoma","glioma","Cancer Biology"],"languages":[],"rights":[],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"https://commons.nmu.edu/theses/100","outbound_label":"Repository record","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Robert Belton, Jr., Ph.D."]},{"key":"dc:creator","label":"Author","values":["Wightman, Samantha M"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.available","label":"Dc Date Available","values":["2016-07-28T07:00:00Z"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Biology"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Thesis"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Master of Science"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["GBM","basigin","BSG","glioblastoma","glioma","Cancer Biology"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["https://commons.nmu.edu/theses/100"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["<p>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. </p>"]},{"key":"dc:title","label":"Title","values":["The Overexpression of Basigin-3 in Glioblastoma"]}]}],"canonical_facts":{"dc:contributor":["Robert Belton, Jr., Ph.D."],"dc:creator":["Wightman, Samantha M"],"dc:date.available":["2016-07-28T07:00:00Z"],"dc:description.abstract":["<p>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. </p>"],"dc:identifier":["https://commons.nmu.edu/theses/100"],"dc:subject":["GBM","basigin","BSG","glioblastoma","glioma","Cancer Biology"],"dc:title":["The Overexpression of Basigin-3 in Glioblastoma"],"thesis:degree_discipline":["Biology"],"thesis:degree_level":["Thesis"],"thesis:degree_name":["Master of Science"]},"updated_at":"2026-07-24T03:23:47Z"}