For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
10
views
21
references
 Top references
cited by
4
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      315
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      The SNP rs4846048 of MTHFR enhances the cervical cancer risk through association with miR‐522: A preliminary report

      research-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Background

          The present research was designed to explore the association between single nucleotide polymorphisms (SNPs) at the 3′‐untranslated region (3′‐UTR) of methylenetetrahydrofolate reductase ( MTHFR) and the risk of cervical cancer (CC).

          Methods

          From May 2015 to October 2016, a total of 197 patients (diagnosed with CC and precancerous lesions, and underwent surgical treatments) were enrolled in the study. Meanwhile, a total of 80 healthy cases were used as the controls. PCR‐DNA analysis was used to explore the genotype of the SNPs (rs4846048 and rs55763075) of the MTHFR 3′‐UTR as well as the association between allelic frequencies and the CC risk. Then, the role of rs4846048 SNPs in the association of microRNA‐522 (miR‐522) and MTHFR was evaluated through luciferase reporter assay. Meanwhile, the modulatory influence of miR‐522 on cell apoptosis and viability of Hela cells was also detected by flow cytometry and MTT assay.

          Results

          The rs4846048 AG and G allele frequencies were significantly higher in CC subgroup compared with the control group. Methylenetetrahydrofolate reductase rs4846048 A/G alleles contributed to miR‐522 binding, and miR‐522 negatively modulated the expressions of MTHFR. Furthermore, miR‐522 overexpression increased cell viability but decreased apoptotic cells in Hela cells.

          Conclusion

          The preliminary report revealed that the SNP rs4846048 of MTHFR enhanced the risk of CC through association with miR‐522, which further regulated cell viability and apoptosis in Hela cells.

          Abstract

          The present research was designed to explore the association between single nucleotide polymorphisms (SNPs) at the 3′‐untranslated region (3′‐UTR) of methylenetetrahydrofolate reductase (MTHFR) and the risk of cervical cancer (CC). This study revealed that the SNP rs4846048 of MTHFR enhanced the risk of CC through association with miR‐522, which further regulated cell viability and apoptosis in Hela cells.

          Related collections

          Most cited references21

          • Record: found
          • Abstract: found
          • Article: not found

          A common mutation in the 5,10-methylenetetrahydrofolate reductase gene affects genomic DNA methylation through an interaction with folate status.

          Simonetta Friso, Sang-Woon Choi, Domenico Girelli … (2002)
          DNA methylation, an essential epigenetic feature of DNA that modulates gene expression and genomic integrity, is catalyzed by methyltransferases that use the universal methyl donor S-adenosyl-l-methionine. Methylenetetrahydrofolate reductase (MTHFR) catalyzes the synthesis of 5-methyltetrahydrofolate (5-methylTHF), the methyl donor for synthesis of methionine from homocysteine and precursor of S-adenosyl-l-methionine. In the present study we sought to determine the effect of folate status on genomic DNA methylation with an emphasis on the interaction with the common C677T mutation in the MTHFR gene. A liquid chromatography/MS method for the analysis of nucleotide bases was used to assess genomic DNA methylation in peripheral blood mononuclear cell DNA from 105 subjects homozygous for this mutation (T/T) and 187 homozygous for the wild-type (C/C) MTHFR genotype. The results show that genomic DNA methylation directly correlates with folate status and inversely with plasma homocysteine (tHcy) levels (P < 0.01). T/T genotypes had a diminished level of DNA methylation compared with those with the C/C wild-type (32.23 vs.62.24 ng 5-methylcytosine/microg DNA, P < 0.0001). When analyzed according to folate status, however, only the T/T subjects with low levels of folate accounted for the diminished DNA methylation (P < 0.0001). Moreover, in T/T subjects DNA methylation status correlated with the methylated proportion of red blood cell folate and was inversely related to the formylated proportion of red blood cell folates (P < 0.03) that is known to be solely represented in those individuals. These results indicate that the MTHFR C677T polymorphism influences DNA methylation status through an interaction with folate status.
          Article 0 comments Cited 180 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Human methylenetetrahydrofolate reductase: isolation of cDNA, mapping and mutation identification.

            Joseph A. Duncan, R Rozen, P Goyette … (1994)
            Methylenetetrahydrofolate reductase (MTHFR) catalyses the reduction of methylenetetrahydrofolate to methyltetrahydrofolate, a cofactor for homocysteine methylation to methionine. MTHFR deficiency, an autosomal recessive disorder, results in homocysteinemia. Using degenerate oligonucleotides based on porcine peptide sequence data, we isolated a 90-bp cDNA by PCR from pig liver RNA. This cDNA was used to isolate a human cDNA, the predicted amino acid sequence of which shows strong homology to porcine MTHFR and to bacterial metF genes. The human gene has been localized to chromosome 1p36.3. Two mutations were identified in MTHFR-deficient patients: a missense mutation (Arg to Gln), in a residue conserved in bacterial enzymes, and a nonsense mutation (Arg to Ter).
            Article 0 comments Cited 128 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              MicroRNA-124 protects against focal cerebral ischemia via mechanisms involving Usp14-dependent REST degradation.

              Barbara C. N. Müller, Eva Bretschneider, Uwe Michel … (2013)
              MicroRNAs (miRNAs) are highly conserved non-coding RNAs modulating gene expression via mRNA binding. Recent work suggests an involvement of miRNAs in cardiovascular diseases including stroke. As such, the brain-abundant miR-124 and its transcriptional repressor RE1-silencing transcription factor (REST) do not only have elementary roles in the developing and the adult brain, but also alter expression upon cerebral ischemia. However, the therapeutic potential of miR-124 against stroke and the mechanisms involved remain elusive. Here, we analyzed the therapeutic potential of ectopic miR-124 against stroke and its underlying mechanisms with regard to the interaction between miR-124 and REST. Our results show that viral vector-mediated miR-124 delivery increased the resistance of cultured oxygen-glucose-deprived cortical neurons in vitro and reduced brain injury as well as functional impairment in mice submitted to middle cerebral artery occlusion. Likewise, miR-124 induced enhanced neurovascular remodeling leading to increased angioneurogenesis 8 weeks post-stroke. While REST abundance increased upon stroke, the increase was prevented by miR-124 despite a so far unknown negative feedback loop between miR-124 and REST. Rather, miR-124 decreased the expression of the deubiquitinating enzyme Usp14, which has two conserved miR-124-binding sites in the 3'UTR of its mRNA, and thereby mediated reduced REST levels. The down-regulation of REST by miR-124 was also mimicked by the Usp14 inhibitor IU-1, suggesting that miR-124 promotes neuronal survival under ischemic conditions via Usp14-dependent REST degradation. Ectopic miR-124 expression, therefore, appears as an attractive and novel tool in stroke treatment, mediating neuroprotection via a hitherto unknown mechanism that involves Usp14-dependent REST degradation.
              Article 0 comments Cited 62 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Contributors
                Jun Wang:
                ORCID: https://orcid.org/0000-0002-7736-2849
                wangjun8963@163.com
                Journal
                Journal ID (nlm-ta): Mol Genet Genomic Med
                Journal ID (iso-abbrev): Mol Genet Genomic Med
                Journal ID (doi): 10.1002/(ISSN)2324-9269
                Journal ID (publisher-id): MGG3
                Title: Molecular Genetics & Genomic Medicine
                Publisher: John Wiley and Sons Inc. (Hoboken )
                ISSN (Electronic): 2324-9269
                Publication date (Electronic): 21 November 2019
                Publication date Collection: January 2020
                Volume: 8
                Issue: 1 ( doiID: 10.1002/mgg3.v8.1 )
                Electronic Location Identifier: e1055
                Affiliations
                [ 1 ] Department of Obstetrics and Gynecology The General Hospital of Northern Theater Command Shenyang Liaoning China
                Author notes
                [*] [* ] Correspondence

                Jun Wang, Department of Obstetrics and Gynecology, General Hospital of Shenyang Military Command, No. 83 Wenhua Road, Shenhe District, Shenyang, Liaoning 110016, China.

                Email: wangjun8963@ 123456163.com

                Author information
                https://orcid.org/0000-0002-7736-2849
                Article
                Publisher ID: MGG31055
                DOI: 10.1002/mgg3.1055
                PMC ID: 6978235
                PubMed ID: 31750632
                SO-VID: b957c3f9-fabd-4da2-86b9-235e7876cef7
                Copyright © © 2019 The Authors. Molecular Genetics & Genomic Medicine published by Wiley Periodicals, Inc.
                License:

                This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

                History
                Date received : 28 October 2018
                Date revision received : 14 October 2019
                Date accepted : 23 October 2019
                Page count
                Figures: 2, Tables: 2, Pages: 8, Words: 5261
                Funding
                Funded by: Natural Science Project of Liaoning Province
                Award ID: 20180551098
                Categories
                Subject: Original Article
                Subject: Original Articles
                Custom metadata
                source-schema-version-number 2.0
                cover-date January 2020
                details-of-publishers-convertor Converter:WILEY_ML3GV2_TO_JATSPMC version:5.7.5 mode:remove_FC converted:23.01.2020

                Keywords: cervical cancer,mir‐522,mthfr,snps
                Data availability:
                Keywords: cervical cancer, mir‐522, mthfr, snps

                Comments

                Comment on this article

                scite_

                Similar content315

                See all similar

                Cited by4

                See all cited by

                Most referenced authors853

                See all reference authors