Examining the Functional Consequences of Tumor Endothelial Marker 8 (TEM8) Expression in Human Breast Cancer Cells
Date
2014-04-17
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Abstract
Tumor Endothelial Marker 8 (TEM8) is a type-1 transmembrane protein overexpressed in tumor associated endothelial cells. Preliminary data from our lab found markedly elevated levels of TEM8 in invasive human breast cancer cell lines of the basal subtype, and reduced TEM8 expression in non-invasive breast cancer cells of the luminal subtype. The functional significance of TEM8 expression in a human breast cancer context is unknown. This thesis explored the consequences of overexpression of TEM8 in non-invasive breast cancer cell lines. MCF7, HTB20, and SKBR3 cells constitutively express low levels of TEM8. The cell lines were infected with lentivirus encoding pLentiTEM8 or control pLentiLacZ. Functional alterations in tumor cell behavior (i.e. viability, apoptosis, adhesion, migration, and invasion) were investigated. NOD-SCID mice were used to evaluate changes in tumor kinetics. In silico data provided by MediSapiens™ was used to assess the prognostic significance of TEM8. The results of this thesis revealed that TEM8 is not sufficient to alter the behavior of non-invasive breast cancer cells to a more malignant phenotype. In vivo studies revealed overexpression of TEM8 does not enhance tumor growth in female NOD-SCID mice. Knocking out host derived TEM8 in MMTV-neu mice had no impact on tumor growth and mortality. In silico data delineate a relationship between TEM8 expression and loco-regional lymphatic spread. The significance of this thesis is that TEM8 alone is not sufficient to cause alterations in the biological behavior of MCF7, HTB20, and SKBR3; however, it may predict loco-regional spread of breast cancer to lymph nodes.
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Oncology
Citation
Sampson, E. (2014). Examining the Functional Consequences of Tumor Endothelial Marker 8 (TEM8) Expression in Human Breast Cancer Cells (Master's thesis, University of Calgary, Calgary, Canada). Retrieved from https://prism.ucalgary.ca. doi:10.11575/PRISM/26027