Investigation of BER repair mechanism enzyme expression changes in prostate cancer

Prostate cancer is one of the most common malignancies in men and ranks second among cancer-related deaths. The incidence and mortality rates of prostate cancer are strongly associated with age, with the highest incidence observed in older men (>65 years). Prostate cancer can be asymptomatic in its early stages and often progresses so slowly that it may only require active surveillance. However, some aggressive forms can metastasize rapidly and lead to mortality. The disease can become more aggressive due to various risk factors such as genetic predisposition, hormones, and environmental factors. Oxidative stress leads to various damages in biomolecules, particularly in DNA. These damages are repaired by specific DNA repair mechanisms in the cell. The base excision repair (BER) mechanism plays a fundamental role in eliminating DNA damage caused by oxidative stress. Enzymes such as APE1, PARP1, XRCC1, UNG, and OGG1 are involved in recognizing, removing, and resynthesizing damaged bases in the BER pathway. In our study, the mRNA expression levels of APE1, PARP1, XRCC1, UNG, and OGG1 were detected in tumor and normal tissues of 50 prostate cancer patients, and the gene expression changes between these two tissues were compared. Additionally, the relationship between the expression levels of these mRNAs and the clinical parameters of the patients was also examined. In our study, gene expression levels were determined using the Quantitative Reverse Transcription Polymerase Chain Reaction (qRT-PCR) method. When the expression levels of the APE1, PARP1, XRCC1, and OGG1 genes in tumor tissues were compared with those in normal tissues, no statistically significant difference was detected (p>0.05). On the other hand, the expression levels of the UNG gene in tumor tissues were found to be significantly increased compared to normal tissues (p=0.02). We hope that our study will contribute to elucidating the relationships between prostate cancer, defects in the BER repair mechanism, and deficiencies in the repair of DNA damage.