The 3'UTR Polymorphisms in the Gene Associated with the Risk of COPD and Their Putative Effects on the microRNA Mechanism.

Evaluating the association between a single nucleotide polymorphism in the 3' untranslated region (3'UTR) of the miRNA binding site of the gene and the occurrence and development of chronic obstructive pulmonary disease (COPD) and providing information to aid in the early detection and treatment of COPD. The regulatory single nuclear polymorphisms (SNPs) located in 3'UTR were searched by using the dbSNP database and miRNA binding site prediction database. Meanwhile, samples from COPD patients and healthy controls in the same period were used for verification. The clinical baseline information of all subjects was collected, and the transcription level and protein expression level of and the expression level of inflammatory factors downstream of were detected. The effects of SNPs' single nucleotide changes on the transcription and expression of inflammatory factors were analyzed. The study included 418 participants (249 in the COPD group and 169 in the control group). SNPs with miRNA binding sites include rs10754558 (G > C), rs1664774076 (ATAT > del), and rs1664775106 (C > G). Furthermore, two genotypes, GCG and GCA, were discovered to have a linkage mutation at 3'UTR 459-461. COPD susceptibility is tightly associated with the expression of the rs1664774076 del/del genotype, and the risk of COPD increased by 2.770 times ( = 0.003). Type 459-461 GCA was substantially related to the likelihood of developing COPD at various stages ( < 0.05). Except for rs10754558, all homozygous mutants increased mRNA and protein levels. had the greatest area under the receiver operating characteristic (ROC) curve for predicting the development and diagnosis of COPD when compared with its downstream inflammatory variables (AUC = 0.9291). The rs1664774076 del/del genotype is a COPD susceptibility gene, and the GCA genotype at 459-461 can be used as an early predictor of COPD exacerbation. The 3'UTR polymorphism may alter the loss of miRNA binding sites, leading to an increase in expression. In the development of COPD, has a better diagnostic value than traditional inflammatory factors. The Clinical Trials Registration number Z: protocol KY01-2020-11-06.