Date of Award
6-1999
Degree Name
Master of Science
Department
Biological Sciences
First Advisor
Dr. Michael McLeod
Second Advisor
Dr. Bruce Bejcek
Third Advisor
Dr. Dave Reinhold
Fourth Advisor
Dr. John Spitsbergen
Access Setting
Masters Thesis-Open Access
Abstract
The hormone Somatostatin (SMS) and its analogs have been shown to mediate a variety of cellular actions including inhibition of cellular growth and differentiation of endocrine tumors such as insulinomas and glucagonomas. The mechanisms by which SMS exerts its antitumorigenic effects are poorly understood but are thought to include one of the five Somatostatin receptors (SSTR1-5), and the protein tyrosine phosphatase SHP-1. To determine if the antiproliferative effects of SMS were due to the presence of the SSTR2 receptor or the stimulation of SHP-1, we introduced cDNA's of the SMS receptor SSTR2, SHP-1, and a dominant negative mutant of SHP-1 into NIH-3T3 cells by lipofection. Our research has shown that the expression of the SSTR2 receptor and the SHP-1 gene product controls cellular proliferation. We have also shown that both the SSTR2 receptor and the SHP-1 gene product can control activation of MAPK proteins. Our results also demonstrate that the SMS analog Sandostatin can control MAPK activation in cells that express the SSTR2 receptor. We therefore conclude that SMS and its analog Sandostatin have different modes of action within the NIH-3T3 mouse fibroblast cell line.
Recommended Citation
Cross, Scott Bradford, "Characterization of NIH-3T3 Mouse Fibroblast Cells Transfected with the Somatostatin Receptor Subtype 2 and the Protein Tyrosine Phosphatase Shp-1" (1999). Masters Theses. 5051.
https://scholarworks.wmich.edu/masters_theses/5051