MicroRNA binding site polymorphism in inflammatory genes associated with colorectal cancer: literature review and bioinformatics analysis

Karimzadeh, Mohammad Reza; Zarin, Maryam; Ehtesham, Naeim; Khosravi, Sharifeh; Soosanabadi, Mohsen; Mosallaei, Meysam; Pourdavoud, Peyman

doi:10.1038/s41417-020-0172-0

Cited by 27 publications

(13 citation statements)

References 149 publications

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“…Inflammation is closely related to the pathogenesis of cancer (72,73) and genetic variations of inflammatory regulators were demonstrated to associate with the increased risk or adverse consequence of several tumors (74)(75)(76)(77)(78)(79).…”

Section: Lbp-snps In Cancermentioning

confidence: 99%

Effects of Lipopolysaccharide-Binding Protein (LBP) Single Nucleotide Polymorphism (SNP) in Infections, Inflammatory Diseases, Metabolic Disorders and Cancers

et al. 2021

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Inflammation, which is induced by the immune response, is recognized as the driving factor in many diseases, including infections and inflammatory diseases, metabolic disorders and cancers. Genetic variations in pivotal genes associated with the immune response, particularly single nucleotide polymorphisms (SNPs), may account for predisposition and clinical outcome of diseases. Lipopolysaccharide (LPS)-binding protein (LBP) functions as an enhancer of the host response to LPS, the main component of the outer membrane of gram-native bacteria. Given the crucial role of LBP in inflammation, we will review the impact of SNPs in the LBP gene on infections and inflammatory diseases, metabolic disorders and cancers.

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Section: Lbp-snps In Cancermentioning

confidence: 99%

Effects of Lipopolysaccharide-Binding Protein (LBP) Single Nucleotide Polymorphism (SNP) in Infections, Inflammatory Diseases, Metabolic Disorders and Cancers

et al. 2021

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“…13,14 Also, several previous studies reported that SNPs located in the 3ˊUTR of mRNA may modulate miRNA-mRNA interactions by impacting the secondary structure of 3ˊUTR and thermodynamic features of the hybridization site; this event, finally, dysregulate the expression of the target gene by changing the binding capacity of miRNAs and consequently predispose the individuals to the disease. 15,16 Ample evidence unveiled that amongst the RA-related genes, those that are involved in the inflammatory response, play a crucial role. The nucleotide oligomerization domain 2 (NOD2) gene is one of the main regulators of chronic inflammatory conditions.…”

Section: Introductionmentioning

confidence: 99%

“…17,22 A review of the literature and miRSNPs databases such as miRdSNP (http://mirdsnp.ccr.buffalo.edu/), MirSNP (http://bioinfo.bjmu.edu.cn/mirsnp/), and Polymirts (http://compbio.uthsc.edu/miRSNP/) databases showed that rs3135500(G>A) and rs3135499(A>C) polymorphisms, located in the 3ˊUTR of NOD2, are in the miRNA binding site or the vicinity of some miRNAs such as miR-192, miR-158, miR-215, miR-98, and miR-573 for rs3135500 and miR-194, miR-3179, miR-3202, miR-4747, and miR-5196 for rs3135499; these polymorphisms could influence on miRNA-mRNA interaction and finally dysregulate gene expression. 15,23 In the current study, for the first time, we evaluated the probable correlations between these two miRNA binding site polymorphisms in the NOD2 gene with the RA risk in the Iranian population. Also, we evaluated the interaction among these polymorphisms and some demographic and laboratory characteristics to find their influence on RA susceptibility and disease activity.…”

Section: Introductionmentioning

confidence: 99%

Association of rs3135500 and rs3135499 Polymorphisms in the MicroRNAbinding Site of Nucleotide-binding Oligomerization Domain 2 (NOD2) Gene with Susceptibility to Rheumatoid Arthritis

Ehtesham¹,

Alani²,

Mortazavi³

et al. 2021

IJAAI

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The nucleotide-binding oligomerization domain 2 (NOD2) is the key regulator of inflammatory responses and has been involved in the pathogenesis of rheumatoid arthritis (RA). Laboratory and in silico evaluations have demonstrated that some polymorphisms in 3ˊUTR of NOD2 gene could influence the secondary structure of this region and similarly thermodynamic features of hybridization site and finally deregulate the expression of NOD2. In the current study, for the first time, we evaluated the possible association between single nucleotide polymorphisms (SNPs) rs3135500 and rs3135499 in the NOD2 gene with RA risk in the Iranian population. One hundred and fifteen patients with RA and 120 healthy subjects were recruited in this case-control study. Genotyping of rs3135500 and rs3135499 polymorphisms were accomplished using the real‑time polymerase chain reaction high resolution melting (HRM) method. We found a substantial association of AA and AG genotypes in rs3135500 with the risk of RA (AA vs GG; OR=5.547; 95%CI [2.564-11.999]; p<0.001 and AG vs GG; OR=2.179; 95%CI [1.145-4.147]; p=0.017). Moreover, in the patient group, there was a significant relationship between the increased concentration of erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) with rs3135500 (A allele) (p<0.05). However, there were no important associations between rs3135499 with the risk of RA (p>0.05). However, we found a noteworthy association of the C allele in rs3135499 with an increased level of CRP in patients (p>0.05). Our findings propose a considerable association between NOD2 polymorphisms with increased risk of RA and disease activity.

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“…MiRNAs are small noncoding RNAs that bind to specific mRNA molecules and cause mRNA degradation or suppression of target gene expression, and they play pivotal roles in the modulation of multiple cellular processes, such as proliferation, differentiation, inflammation and apoptosis 41 . Increasing evidence has demonstrated the important impact of specific genetic variations within the 3′-UTR on the binding of miRNAs to cause the gain or loss of regulation by certain miRNAs, ultimately resulting in susceptibility to multiple diseases 42 , 43 . According to bioinformatics analyses predicted by miRNASNP-v3 ( http://bioinfo.life.hust.edu.cn/miRNASNP/ ) and a previous study 27 , 38 , the 29940 G-to-C mutation in the 3′-UTR of NLRP3 might establish a new functional binding site for miR-146a-5p, which contributes to potential miR-146-5p recruitment and binding.…”

Section: Discussionmentioning

confidence: 99%

A gain-of-function NLRP3 3′-UTR polymorphism causes miR-146a-mediated suppression of NLRP3 expression and confers protection against sepsis progression

Chen²,

Hong

et al. 2021

Sci Rep

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Nucleotide-binding domain and leucine-rich repeat (LRR)-containing family protein 3 (NLRP3) regulated the maturation of inflammation-related cytokines by forming NLRP3 inflammasome, which plays pivotal roles in sepsis pathogenesis. In this study, we evaluated the genetic association of NLRP3 polymorphisms with sepsis (640 patients and 769 controls) and characterized the impact of NLRP3 polymorphisms on NLRP3 expression and inflammatory responses. No significant differences were observed in genotype/allelic frequencies of NLRP3 29940G>C between sepsis cases and controls. The G allele was significantly overrepresented in patients with septic shock than those in sepsis subgroup, and the GC/GG genetypes were related to the 28-day mortality of sepsis. Lipopolysaccharide challenge to peripheral blood mononuclear cells showed a significant suppression of NLRP3 mRNA expression and release of IL-1β and TNF-α in CC compared with the GC/GG genotype category. Functional experiments with luciferase reporter vectors containing the NLRP3 3′-UTR with the 29940 G-to-C variation in HUVECs and THP-1 cells showed a potential suppressive effect of miR-146a on NLRP3 transcription in the presence of the C allele. Taken together, these results demonstrated that the 29940 G-to-C mutation within the NLRP3 3′-UTR was a gain-of-function alteration that caused the suppression of NLRP3 expression and downstream inflammatory cytokine production via binding with miR-146a, which ultimately protected patients against susceptibility to sepsis progression and poor clinical outcome.

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MicroRNA binding site polymorphism in inflammatory genes associated with colorectal cancer: literature review and bioinformatics analysis

Cited by 27 publications

References 149 publications

Effects of Lipopolysaccharide-Binding Protein (LBP) Single Nucleotide Polymorphism (SNP) in Infections, Inflammatory Diseases, Metabolic Disorders and Cancers

Effects of Lipopolysaccharide-Binding Protein (LBP) Single Nucleotide Polymorphism (SNP) in Infections, Inflammatory Diseases, Metabolic Disorders and Cancers

Association of rs3135500 and rs3135499 Polymorphisms in the MicroRNAbinding Site of Nucleotide-binding Oligomerization Domain 2 (NOD2) Gene with Susceptibility to Rheumatoid Arthritis

A gain-of-function NLRP3 3′-UTR polymorphism causes miR-146a-mediated suppression of NLRP3 expression and confers protection against sepsis progression

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