印度人群AR、PSA (KLK)和ER-β基因变异与良性前列腺增生(BPH)发病机制分析

A. Prajapati, Gaurav Chauhan, Sharad Gupta, P. Pandya, Sukhbir Kaur, Sarita Gupta
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摘要

良性前列腺增生(BPH)的发病机制在基因组中表现出个体差异,类固醇激素基因AR、PSA (KLK)和ER-β的多态性在改变BPH疾病进展率方面具有深远的影响。AR中的1754 A/G外显子-1、PSA(KLK)中的启动子-158 A/G和ER-β中外显子-8中的1730 A/G 3'UTR的单核苷酸多态性(snp)与BPH的发病有关。本研究分析了印度人群ER-β基因外显子8中的AR-1754 A/G外显子1、PSA-ARE1启动子-158 A/G和1730 A/G 3'UTR。采用PCR、RFLP-PCR和基因型-表型相关性分析BPH患者和健康人群的多态性。在研究中,与对照组相比,AR和ER-β snp与BPH发病机制有显著相关性[55.7% (OR 3.0 (95% CI 1.67-5.46) (p 0.0002)]和[52.6% (OR 6.5, 95% CI 3.27-12.74) (p 0.0001)]。这两种多态性都表明G等位基因与BPH发病风险增加有关。PSA的A/G基因型频率为54%,与BPH的发病机制无关。进一步的基因型-表型相关研究证明基因-基因相互作用在BPH的病因学中起重要作用。虽然发病的易感性不能依赖于单一或少数遗传变异,但值得注意的是,AR、PSA和ER-β变异与BPH的发病具有全球相关性。因此,印度人群中较高频率的AR和ER-β变异可能是BPH发病的关键。
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Analysis of AR, PSA (KLK) and ER-β genetic variants and Benign Prostate Hyperplasia (BPH) pathogenesis in Indian population
Benign Prostate Hyperplasia (BPH) pathogenesis exhibitsinter-individual variation in the genome as polymorphisms in the steroid hormone genes AR, PSA (KLK) and ER-β profound effects in altering BPH disease progression rate. Single nucleotide polymorphisms (SNPs) designated 1754 A/G exon-1 in AR, Promotor-158 A/G in PSA(KLK) and 1730 A/G 3’UTR in Exon-8 in ER-β have been associated with BPH pathogenesis. In the current study, AR-1754 A/G exon-1, PSA-ARE1 Promotor-158 A/G and 1730 A/G 3’UTR in Exon-8 in ER-β were analysed in Indian population.The polymorphisms in BPH patients and healthy individuals were evaluated by PCR, RFLP–PCR and genotype–phenotype correlation. In the study AR and ER-β SNPs demonstrated significant association [55.7% (OR 3.0 (95% CI 1.67–5.46) (p 0.0002)] and [52.6 % (OR 6.5, 95% CI 3.27–12.74) (p 0.0001)] with BPH pathogenesis in patients as compared to control. With both the polymorphisms indicating a trend towards an association of the G allele with an increased risk of BPH pathogenesis. The A/G genotype frequency of PSA was 54 % in patients and was not associated with BPH pathogenesis. Further genotype–phenotype correlation study has provided evidence that gene–gene interactions play an important role in the etiology of BPH. Although susceptibility to pathogenesis cannot be dependent on a single or small number of genetic variants, it is noteworthy that AR, PSA and ER-β variants have been correlated globally with BPH pathogenesis. Hence, the higher frequency of AR and ER-β variants in the Indian population may be critical in BPH pathogenesis.
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