Date of Award

Summer 6-12-2019

Degree Type

Thesis

Degree Name

MSOB (Master of Science in Oral Biology)

Abstract

To gain a better understanding of the tumorigenesis of Kaposi sarcoma (KS) it is essential to understand the role KSHV plays in the mesenchymal-to endothelial transition (MEndT). PROX1 in human related cancers can act as a transcriptional repressor or activator that leads to several effects on cellular differentiation and proliferation1-3. PROX1 upregulation may play a significant role in the MEndT and in turn effect the tumorigenesis of KS. This study was conducted to evaluate if PROX1 is upregulated by KSHV. To test this, human GMSCs and human PDLSCs were used, as well as 293T cells. They were transfected at 70% confluency using Lipofectamine 3000 with a PROX1 promoter, pPROX1, cloned into a pGL3 promoter. The cells were then infected using recombinant green fluorescent protein (GFP) expressing KSHV (rKSHV.219) . A luciferase assay was conducted to measure expression of pPROX1. The samples were lysed and collected at different time points (24, 36, 48 hours). Results show that in 293Tcells KSHV infected cells do not exhibit noticeable luciferase signal activation of pPROX1 at 24, 36, and 48 hours post infection, PDLSCs show a slight increase in luciferase signal in KSHV+ pGL3-PROX1 v6 is at 24, 36 and 48 hours post infection, while in KSHV infected GMSCs do not exhibit noticeable luciferase signal activation of pPROX1 at 24,36 and 48 hours. In conclusion, there is no significant activation of pPROX1 in KSHV infected 293Tcells, PDLSCs, and GMSCs. Future experiments that are warranted would be assessing the upregulation of PROX1 via Western Blot and RT-PCR.

Included in

Dentistry Commons

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