Association between COX-2 -1195G&gt;A polymorphism and gastrointestinal cancer risk: A meta-analysis

Zhang, Xiaowei; Li, Jun; Jiang, Yuxing; Chen, Yuxiang

doi:10.3748/wjg.v23.i12.2234

Cited by 5 publications

(3 citation statements)

References 48 publications

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“…This result was also similar to reports investigating different cancers. It was previously demonstrated that the AA genotype in the COX-2 –1195G>A gene polymorphism might be an important predisposing factor for gastric cancers in Asian patients [13] and esophageal cancer patients [14].…”

Section: Discussionmentioning

confidence: 99%

Cyclooxygenase-2 Gene Polymorphisms –765G>C and –1195A>G and Mycosis Fungoides Risk

et al. 2019

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Background: Cyclooxygenase-2 (COX-2) is an inducible modulator of inflammation that acts through increasing prostaglandin levels and has been described as a major mediator linking inflammation to cancer. Previous studies supported that COX-2–765G>C and –1195A>G polymorphisms were associated with increased risk of several solid tissue cancers as well as some hematological malignancies. Objective: The aim of the study was to elucidate the association between functional COX-2 genotypes (–765G>C and –1195A>G) polymorphisms and the risk of developing mycosis fungoides (MF). Methods: This was a hospital-based, case-control study of 70 MF patients and 100 MF-free controls. We genotyped COX-2 –1195A>G, –765G>C, and –8473T>C polymorphisms by using the PCR-restriction fragment length polymorphism method. Results: The AA genotype in the COX-2 –1195A>G gene polymorphism and the GC genotype in the COX-2 −765G>C gene were significantly more frequent among MF patients compared to controls (p< 0.001 and p = 0.002, respectively). Conclusion: The results indicate a possible role of COX-2 genes in the pathogenesis of MF. These novel findings may allow for notable future advances, as it will enable the identification of the individuals most susceptible to MF.

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Section: Discussionmentioning

confidence: 99%

Cyclooxygenase-2 Gene Polymorphisms –765G>C and –1195A>G and Mycosis Fungoides Risk

et al. 2019

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“…Post-transcriptional regulation of PTGS2 occurs through a complex interplay of specific trans-acting RNA-binding proteins and microRNAs (miRs) [11][12][13][14], including miR-146a-5p (miR-146a) [15][16][17]. Functional polymorphisms in the PTGS2 gene have been extensively investigated [18,19], which modulate the risk of various cancers [20][21][22]. Previously, we evaluated the influence of PTGS2 gene polymorphism rs20417G>C in melanoma, observing that it was significantly associated with an increased risk [23].…”

Section: Introductionmentioning

confidence: 99%

Sex-dependent interaction of PTGS2 with miR-146a as risk factor for melanoma and the impact of sex hormones in gene expression in skin cells

Orlandi,

Ceccuzzi,

Belpinati

et al. 2024

Melanoma Research

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Gender disparity in melanoma is a complex issue where sex hormones could be engaged. Differences in genetic variations are important in understanding the mechanisms of sex disparity in melanoma. Post-transcriptional regulation of prostaglandin-endoperoxide synthase (PTGS2) mRNA occurs through a complex interplay of specific trans-acting RNA-binding proteins and microRNAs. MiR-146a is a key player in melanoma, modulating immune responses and tumor microenvironment (TME). Polymorphisms in PTGS2 gene rs20415G<C and miR-146a gene rs2910164G>C have been associated with an increased risk of melanoma. Epistasis between polymorphisms rs20415G<C and rs2910164G>C was investigated by genotyping 453 melanoma patients and 382 control individuals. The effects of testosterone and 17β-estradiol were analyzed in keratinocytes and two melanoma cell lines. The rs2910164GG showed a higher risk in the presence of the genotype rs20417CC in the male population. Testosterone and 17β-estradiol act differently on PTGS2 and miR-146a expression, depending on the cell type. Testosterone augments PTGS2 gene expression in keratinocytes and miR-146a in melanoma cells. While 17β-estradiol only increases miR-146a expression in HaCaT cells. The present study indicates a sex-specific relation between miR-146a and PTGS2 polymorphisms with melanoma cancer risk. Testosterone and 17β-estradiol act differently on the expression of PTGS2 and miR-146a depending on the skin cell type.

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“…This SNP can also establish E2 promoter binding factor 1 (E2F1), which can enhance COX-2 transcription. COX-2 transcription is a complicated process that depends on the type of cell and type of stimulus (cytokine, growth factor, or bacterial endotoxins) (14,15). The objective of this study was to evaluate the prevalence of -765G>C (rs20417) polymorphism in a group of Iraqi patients with UC and its correlation with the clinical severity of the disease.…”

Section: Introduction Introductionmentioning

confidence: 99%

Impact of Cyclooxygenase-2 Polymorphism -765G>C (rs20417) on the Development of Ulcerative Colitis

Alahmed,

A. Al-Rubaee

2023

SGO

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Background: Ulcerative Colitis is chronic, progressive disease affecting large intestine. Cyclooxygenase-2 enzyme is an inducible enzyme that has important role in the process of inflammation. Ulcerative Colitis pathogenesis is comprising chronic inflammation; any alteration in the gene responsible for cuclooxygenase-2 expression such as -765G>C (rs20417) polymorphism may affect risk of having the disease. Objectives: To record and evaluate the prevalence of -765G>C (rs20417) polymorphism in group of Ulcerative Colitis Iraqi patients and correlation it with disease clinical severity. Method: A case-control, single-center study included ninety participants collected from Gastroenterology and Hepatology Hospital/Basrah/Iraq, divided in to 30 newly diagnosed patients, 30 previously diagnosed patients and 30 healthy controls. Genetic analysis done through dual color discrimination assay. Results: To our knowledge the present study is the first report in Iraqi population that investigates the correlation between COX-2 polymorphism, rs20417 with risk of developing UC. The prevalence of the -765G and -765C alleles was 85.8% and 14.1% in the patient group and 86.6% and 13.3% in the control group respectively, the -765CC variant in Basrah city was infrequent in population of UC patients (14.1%) and in controls (13.3%). There was no statistical difference in the disease association and in the relationship to the disease severity but GG genotypes showed more sever clinical disease than those with other variants. Conclusion:In disparity to other reports on the role of COX-2 polymorphisms at position -765 in the term of modifying the risk for UC in a group of Arab Iraqi patients, we did not find significant results for this variation's association but in term of association with the level of disease clinical severity, carriers of GG wild type had more active clinical disease than those with mutant variants.

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Association between COX-2 -1195G>A polymorphism and gastrointestinal cancer risk: A meta-analysis

Cited by 5 publications

References 48 publications

Cyclooxygenase-2 Gene Polymorphisms –765G>C and –1195A>G and Mycosis Fungoides Risk

Cyclooxygenase-2 Gene Polymorphisms –765G>C and –1195A>G and Mycosis Fungoides Risk

Sex-dependent interaction of PTGS2 with miR-146a as risk factor for melanoma and the impact of sex hormones in gene expression in skin cells

Impact of Cyclooxygenase-2 Polymorphism -765G>C (rs20417) on the Development of Ulcerative Colitis

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Association between COX-2 -1195G>A polymorphism and gastrointestinal cancer risk: A meta-analysis

Cited by 5 publications

References 48 publications

Cyclooxygenase-2 Gene Polymorphisms –765G&#x3e;C and –1195A&#x3e;G and Mycosis Fungoides Risk

Cyclooxygenase-2 Gene Polymorphisms –765G&#x3e;C and –1195A&#x3e;G and Mycosis Fungoides Risk

Sex-dependent interaction of PTGS2 with miR-146a as risk factor for melanoma and the impact of sex hormones in gene expression in skin cells

Impact of Cyclooxygenase-2 Polymorphism -765G>C (rs20417) on the Development of Ulcerative Colitis

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Cyclooxygenase-2 Gene Polymorphisms –765G>C and –1195A>G and Mycosis Fungoides Risk

Cyclooxygenase-2 Gene Polymorphisms –765G>C and –1195A>G and Mycosis Fungoides Risk