Abstract
In this study mitochondrial D-Loop variations in Iranian prostate cancer and benign prostatic hyperplasia (BPH) patients were investigated. Tumour samples and corresponding non-cancerous prostate tissue from 40 prostate cancer patients and 40 age-matched BPH patients were collected. The entire mtD-loop region (16024-576) was amplified using the PCR method and products were gel-purified and subjected to direct nucleotide sequencing. A total of 129 variations were found, the most frequent being 263A-G and 310T-C among both BPH and prostate cancer patients. Variation of 309 C-T was significantly more frequent in prostate cancer patients (P value<0.05). Four novel variations were observed on comparison with the MITOMAP database. Novel variations were np16154delT, np366G-A, np389G-A and 56insT. There was no correspondence between the different variations and the age of subjects. Considering that D-loop variations were frequent in both BPH and prostate cancer patients in our study, the fact that both groups had high average age can be a possible contributing factor. D-loop polymorphisms and microsatellite instability can influence cell physiology and result in a benign or malignant phenotype. Significantly higher frequency of 309 C-T variation in cancer patients is a notable finding and must be a focus of attention in future studies.
Highlights
Prostate cancer is one of the most common malignancies among men over the age of 55 and is responsible for about 6% of all male cancer deaths (Parkin et al, 2001)
Mitochondrion plays an essential role in different pathways in the cell such as energy production, reactive oxygen species (ROS) generation, and in a fundamental biological process in which cells die in a controlled manner called apoptosis
Diagnosis of prostate cancer and benign prostatic hyperplasia (BPH) was made by an elevated serum level of prostate specific antigen (PSA) and transrectal ultrasound-guided biopsies (TRUS)
Summary
Prostate cancer is one of the most common malignancies among men over the age of 55 and is responsible for about 6% of all male cancer deaths (Parkin et al, 2001). Prostate cancer patients in our study, the fact that both groups had high average age can be a possible contributing factor. In contrast in another study there was no association between mitochondrial haplogroups and control region polymorphisms with prostate cancer (Mueller et al, 2009). In spite of a limited number of publication data on mitochondrial DNA, there are controversial results of investigating mtDNA variations in prostate cancer.
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