Defense Date

2024

Document Type

Thesis

Degree Name

Master of Science

Department

Human and Molecular Genetics

First Advisor

Zheng Fu

Second Advisor

Jolene Windle

Third Advisor

Jiong Li

Abstract

Prostate cancer is the leading cause of cancer-related deaths among men worldwide, and the development of resistance to existing treatments necessitates the exploration of new therapeutic strategies, including combination therapies. This study investigates the role of Polo-like kinase 1 (PLK1), located on chromosome 16p12.2, as an oncogene in prostate cancer. We generated a transgenic mouse model with prostate-specific overexpression of PLK1 to closely mimic human prostate cancer progression. Quantitative PCR (qPCR) analysis was employed to characterize the molecular profile of PLK1, revealing its implication in multiple pathways. To further elucidate the functional consequences of PLK1 overexpression, we confirmed phenotypic progression using immunohistochemistry (IHC) and hematoxylin and eosin (H&E) staining, which supported our hypothesis that PLK1 overexpression accelerates prostate cancer progression. This model offers a valuable tool for investigating the specific contributions of PLK1 to prostate cancer and identifying opportunities for targeted therapeutic strategies. Future research will focus on comprehensive functional assays, in vivo tumorigenesis studies, and the potential of PLK1 inhibitors as a therapeutic option for prostate cancer.

Rights

© The Author

Is Part Of

VCU University Archives

Is Part Of

VCU Theses and Dissertations

Date of Submission

12-12-2024

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