Date of Submission

2024

Document Type

Thesis

Department

Biology and Environmental Sciences

Advisor

Eva Sapi, Ph.D.

Keywords

Polymerase Beta, Cancer Development, Breast Cancer, Borrelia burgdorferi

MeSH

Breast Neoplasms, Borrelia burgdorferi, Neoplasm Invasiveness

LCSH

Breast--Cancer--Research, Borrelia burgdorferi, Cancer cells--Growth

Abstract

Polymerase beta (Polβ) is a DNA repair enzyme with a critical role in the base excision repair pathway and the maintenance of genomic stability. Altered expression and specific splice variants of Polβ have been widely associated with cancer development. Recent studies have also linked bacterial infections and inflammation to aberrant Polβ activity, contributing to tumorigenesis. Borrelia burgdorferi, the causative agent of Lyme disease, has been shown to invade breast cancer cells, disrupting gene expression and affecting pathways essential for genomic stability. However, no studies to date have specifically investigated the effects of B. burgdorferi infection on Polβ in breast cancer cells.

This thesis addresses this gap by examining the impact of B. burgdorferi infection on Polβ expression and splice variants in MDA-MB-231 breast cancer cells using standard PCR and Real-Time quantitative PCR (RT-qPCR). The findings revealed no detectable splice variants but demonstrated a significant 2.5-fold increase in Polβ expression in Borrelia-infected breast cancer cells compared to uninfected cells. These results provide novel insights into the potential impact of B. burgdorferi on Polβ function in breast cancer, highlighting the need for further research to understand the significance of these findings.

Available for download on Tuesday, December 18, 2029

Share

COinS