Northern Michigan University
EFFECTS OF LEPTIN ON ESTABLISHED GLIOBLASTOMA CELL LINES
Abstract
dc:description.abstract<p>Glioblastoma is one of the most difficult cancers to treat because it is aggressive and resistant to therapy. The discovery of new therapeutic targets is drastically needed as zero improved treatment options have been added to the standard of care over the past 15 years. New and promising therapeutic targets are arising from psychosocial and environmental enrichment studies examining the role of stress in cancer progression. In animal models, eustress appears to slow tumor growth and recurrence resulting in increased overall survival and progression free survival while distress is associated with decreased overall survival. The cellular pathways activated by eustress were examined in glioblastoma cell lines; leading us to examine the use of β<sub>3</sub> adrenergic stimulation to decrease leptin gene expression as a possible novel therapeutic. The role of leptin and β<sub>3 </sub>adrenergic stimulation were examined using a cell viability assay to assess changes in proliferation and quantitative PCR to assess gene expression. With the use of a selective β<sub>3 </sub>agonist, leptin and leptin receptor mRNA was down regulated and resulted in decreased cell proliferation. Leptin’s observed role in glioblastoma cell proliferation and survival was supported by treatments with a leptin antagonist, resulting in decreased cellular proliferation. This evidence would suggest further examination of leptin as a therapeutic target for glioblastoma.</p>
Degree
thesis:*- Name thesis:degree_name
- Master of Science
- Level thesis:degree_level
- Thesis
- Discipline thesis:degree_discipline
- Biology
- Year dc:date.available
- 2014
Author and committee
dc:creator, dc:contributor.*- Author dc:creator
-
- Cook, Nicholas J
- Contributors dc:contributor
-
- Dr. Robert Winn
Subjects
dc:subject × 6Identifiers
dc:identifier.*- Repository record dc:identifier
- https://commons.nmu.edu/theses/23
- OAI identifier oai:identifier
- oai:commons.nmu.edu:theses-1030