EVALUATION OF THE RELATIONSHIP BETWEEN GENETIC POLYMORPHISMS AND GENE EXPRESSION OF THE KLK3 GENE IN SUSCEPTIBILITY TO BENIGN PROSTATIC HYPERPLASIA IN IRAQI PATIENTS

Abstract

Abstract
Prostatic hyperplasia is an anatomical enlargement of the prostate gland that affects men with age and leads to more annoying urinary symptoms than a serious disease. The causes of this disease are not yet fully known, but some androgenic hormones may play a role in this. The testosterone hormone is converted into the compound dihydrotestosterone, and the effect of this compound on the prostate leads to The importance of prostate gland hyperplasia lies in its causing an anatomical obstruction in the neck of the bladder, which controls the mechanism of expelling urine out of the body, and if not treated, it leads to urine retention in the bladder and ureters, where in the final stages, hydronephrosis occurs and enlarged kidneys after obstruction of the urethra, and if this hydronephrosis continues for a long time, it leads to functional insufficiency of the kidneys. The current study aimed to evaluate the role of genetic polymorphism and gene expression in the KLK3 gene at the variant locus of rs2271095, rs11573 is a gene located on chromosome 19 that mainly encodes for enzymes that have a role in prostate endothelial hyperplasia by increasing the gene expression of the gene. The results of the current study showed that there is no genetic heterogeneity at the rs2271095 variant site. The TT homozygous genotype and the T allele are considered a causative factor, with an odds ratio of 2.05 and 1.56, respectively. According to Fisher's probability P=0.666, so this genotype C and its allele C is an etiologic factor according to the odds values of 1.00 and 0.64, respectively, noting that the different proportions for genotypes and their alleles due to the small sample size. As for the differential genotype TC, according to Fisher's probability P=0.205, the genotype CT and allele C is a protective factor for the disease according to the odds values of 0.40 and 0.64, respectively. There are no statistically significant differences between the observed and predicted values of the three genotypes and alleles, with Hardy-Weinberg likelihood values of 0.3437 and 0.0154 in the patient and healthy group, respectively. rs11573 heterozygous site according to Fisher's likelihood (P = 0.268) between patients and healthy people. The homozygous TT and T allele genotypes were considered as an etiologic factor with an odds ratio of 1.96 and 1.48, respectively. According to Fisher's probability P=0.666, so this genotype CC and its C allele is a protective factor for the disease according to the likelihood values of 1.00 and 0.68, respectively. According to Fisher's probability P=0.253, so this genotype CT and its C allele is a protective factor for the disease according to the likelihood values of 0.49 and 0.68, respectively. The results showed that the distribution of the three genotypes of TT, CT, CC and the allelic frequency of the KLK3 gene at the rs11573 T/A/C variant site in the study population according to Hardy-Weinberg's law is balanced, as there are statistically significant differences between the observed and expected values of the three genotypes and the nights, as the Hardy-Weinberg probability value was 0.9926 NS and 0.2001 NS in the patient and healthy group, respectively. The results of the current study show high levels of gene expression of the KLK3 gene in BPH patients compared to healthy people, as the real time PCR results showed a difference in the CT values of the patient group compared to the control group and the CT values were lower in patients compared to the control group and the folding level in patients (9.04±3.91) was higher than healthy people (1.00±0.00) with statistically significant differences (P<0.001***) and high statistical significance (P<0.001***).