Changes in TP53 gene, telomere length, mitochondrial DNA, and its amount in benign prostatic hyperplasia patients

Benign prostatic hyperplasia (BPH) is a growing issue due to an ageing population; however, there are not enough studies connecting it with ageing hallmarks. Some of the ageing hallmarks are changes in telomere length (TL) and genetic changes like possible mutations in the TP53 gene or mitochondrial genome (mtDNA). Our study investigated these factors to see if they could be linked with BPH. Prostate tissue samples were obtained from 32 patients with BPH (and 30 blood samples). As a healthy control group, age-matching blood DNA samples were used. For mtDNA sequence data comparison, 50 samples of a general Latvian population were used. The full mtDNA genome was sequenced using Next Generation Sequencing (NGS), for TP53 gene - Sanger sequencing, and for mtDNA amount and telomere length - qPCR assay. BPH patients in prostate tissue had much higher TL than in blood cells, and the healthy controls had the shortest telomeres. Also, the mtDNA amount in BPH prostate tissue was the highest compared with blood, and controls had the smallest amount. In the TP53 gene, we did not find any mutations that could be linked to BPH. In the mtDNA genome, we found several unique mutations and heteroplasmic changes, as well as changes that have been linked before with prostate cancer (PC). In conclusion, prolonged telomeres and changes in mtDNA amount might be involved in the development of BPH. Concerning mtDNA genome changes, some of the heteroplasmic or homoplasmic variants might contribute to the development of BPH. More studies should be conducted to prove or disapprove of these connections.