Upregulation of Uracil DNA Glycosylase (UNG) in Prostate Cancer

Prostate cancer is the second most common malignancy and a major cause of cancerrelated deaths in men. Dysregulation of DNA repair mechanisms, particularly those involved in base excision repair (BER), contributes significantly to carcinogenesis. Alterations in this pathway have been linked to aggressive tumor behavior, early recurrence, and poor survival, positioning DNA repair as a promising therapeutic target. This study focused on the expression of two BER genes, uracil DNA glycosylase (UNG) and 8-oxoguanine DNA glycosylase (OGG1), in tumor and adjacent normal prostate tissues. Fifty prostate cancer patients were enrolled. Tumor and adjacent normal tissues were obtained using tru-cut biopsy. Gene expression levels of UNG and OGG1 were assessed by quantitative real-time PCR. UNG expression was significantly elevated in tumor tissues compared to normal tissues, showing a 3.39-fold increase (p = 0.02). OGG1 expression also increased by 2.60-fold, but this was not statistically significant (p > 0.05). A positive correlation was observed between UNG expression and PSA levels in tumor tissues (r = 0.341, p = 0.01). No statistically significant difference in gene expression was found between tumor and normal tissues with respect to clinical parameters such as diabetes, hypertension, PIRADS score, Gleason score, smoking status, or presence of nodules. UNG is significantly upregulated in prostate cancer and may help maintain genomic stability and tumor cell survival. Targeting UNG alongside DNA-damaging therapies could disrupt cancer progression. Further studies on BER genes may support personalized treatment approaches in prostate cancer.