test Browse by Author Names Browse by Titles of Works Browse by Subjects of Works Browse by Issue Dates of Works

Advanced Search
& Collections
Issue Date   
Sign on to:   
Receive email
My Account
authorized users
Edit Profile   
About T-Space   

T-Space at The University of Toronto Libraries >
School of Graduate Studies - Theses >
Master >

Please use this identifier to cite or link to this item: http://hdl.handle.net/1807/25551

Title: Alterations in Tgf-β Signaling Mediate the Biologic Behaviour of Osteosarcoma Cell Lines
Authors: Deheshi, Benjamin Michael
Advisor: Wunder, Jay
Department: Medical Science
Keywords: Osteosarcoma
Issue Date: 31-Dec-2010
Abstract: Osteosarcoma is a mesenchymal tumour of bone common among children and young adults. Prognosis is poor if metastases are present at diagnosis. The transforming growth factor beta (TGF-β) signaling pathway plays a complex dual role in cancer. We hypothesized that alterations in the TGF-β signaling pathway are important in the tumorigenesis of osteosarcoma cell lines. Smad phosphorylation and nuclear localization, Smad4 expression, and TAZ expression were determined in the HOS osteosarcoma cell line and tumorigenic derivatives. Basal TGF-β activity and TAZ expression correlated with a tumorigenic phenotype in the KHOS cell lines as measured by Anchorage Independent Growth (AIG). In comparison, exogenous TGF-β suppressed AIG and acted as a tumour suppressor, while Smad4-deficient KHOS cells were resistant to the inhibitory TGF-β effect. In conclusion, basal TGF-β signaling and TAZ correlate with increased tumorigenic potential in osteosarcoma cell lines, whereas exogenous TGF-β acted as a tumour suppressor in a Smad4-dependent manner.
URI: http://hdl.handle.net/1807/25551
Appears in Collections:Master
Institute of Medical Science - Master theses

Files in This Item:

File Description SizeFormat
Deheshi_Benjamin_M_201011_MSc_thesis.pdf5.25 MBAdobe PDF

This item is licensed under a Creative Commons License
Creative Commons

Items in T-Space are protected by copyright, with all rights reserved, unless otherwise indicated.