Award Date

5-1-2025

Degree Type

Thesis

Degree Name

Master of Science (MS)

Department

Dental Medicine

First Committee Member

Karl Kingsley

Second Committee Member

Brian Chrzan

Third Committee Member

Katherine Howard

Fourth Committee Member

Louisa Messenger

Number of Pages

52

Abstract

Many health benefits are associated with Vitamin D (VitD), although deficiency is associated with poor health outcomes and increased risk for cancer development. For example, many tissue specific enzymes are involved in VitD metabolism, and mutations or deletions within Vitamin D receptor (VDR) genes are known to increase cancer risk by altering their functions or bioavailability, although less is known about these phenomena in oral cancers. Using well characterized, commercially available oral cell lines (OKF4, HGF-1, SCC4, SCC9, SCC15, SCC25, CAL27), mRNA expression of P450 cytochrome VitD metabolic enzymes and receptor genes by qPCR revealed differential results. One oral cancer line (SCC15) did not express either receptor or entry genes VDR or FOK1 and was also least affected by VitD3 administration in growth assays. In contrast, most oral cancers were missing one or more hydrolase (CYP2R1,CYP24A1) or hydrolate (CYP27A1, CYP27B1) enzymes. SCC25 was missing both hydrolate enzymes and was the most inhibited in VitD3 growth assays, while SCC4 was missing both hydroxylase enzymes and was the least inhibited by VitD2. These associations between mRNA expression (or lack thereof) and VitD3 and VitD2 responsiveness identify molecular targets, which may lead to effective screening tools for VitD-related complementary and alternative therapies.

Keywords

oral cancer; Vitamin D

Disciplines

Cell Biology

File Format

pdf

File Size

745 KB

Degree Grantor

University of Nevada, Las Vegas

Language

English

Rights

IN COPYRIGHT. For more information about this rights statement, please visit http://rightsstatements.org/vocab/InC/1.0/

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