For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
7
views
35
references
 Top references
cited by
16
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      724
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Association between METTL3 gene polymorphisms and neuroblastoma susceptibility: A nine‐centre case‐control study

      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

          Neuroblastoma ranks as the most commonly seen and deadly solid tumour in infancy. The aberrant activity of m 6A‐RNA methyltransferase METTL3 is involved in human cancers. Therefore, functional genetic variants in the METTL3 gene may contribute to neuroblastoma risk. In the current nine‐centre case‐control study, we aimed to analyse the association between the METTL3 gene single nucleotide polymorphisms (SNPs) and neuroblastoma susceptibility. We genotyped four METTL3 gene SNPs (rs1061026 T>G, rs1061027 C>A, rs1139130 A>G, and rs1263801 G>C) in 968 neuroblastoma patients and 1814 controls in China. We found significant associations between these SNPs and neuroblastoma risk in neither single‐locus nor combined analyses. Interestingly, in the stratified analysis, we observed a significant risk association with rs1061027 AA in subgroups of children ≤ 18 months of age (adjusted OR = 1.87, 95% CI = 1.03‐3.41, P = .040) and females (adjusted OR = 1.86, 95% CI = 1.07‐3.24, P = .028). Overall, we identified a significant association between METTL3 gene rs1061027 C>A polymorphism and neuroblastoma risk in children ≤18 months of age and females. Our findings provide novel insights into the genetic determinants of neuroblastoma.

          Related collections

          Most cited references35

          • Record: found
          • Abstract: found
          • Article: found
          Is Open Access

          METTL3 facilitates tumor progression via an m 6 A-IGF2BP2-dependent mechanism in colorectal carcinoma

          Ting Li, Pei-Shan Hu, Zhixiang Zuo … (2019)
          Background Colorectal carcinoma (CRC) is one of the most common malignant tumors, and its main cause of death is tumor metastasis. RNA N6-methyladenosine (m6A) is an emerging regulatory mechanism for gene expression and methyltransferase-like 3 (METTL3) participates in tumor progression in several cancer types. However, its role in CRC remains unexplored. Methods Western blot, quantitative real-time PCR (RT-qPCR) and immunohistochemical (IHC) were used to detect METTL3 expression in cell lines and patient tissues. Methylated RNA immunoprecipitation sequencing (MeRIP-seq) and transcriptomic RNA sequencing (RNA-seq) were used to screen the target genes of METTL3. The biological functions of METTL3 were investigated in vitro and in vivo. RNA pull-down and RNA immunoprecipitation assays were conducted to explore the specific binding of target genes. RNA stability assay was used to detect the half-lives of the downstream genes of METTL3. Results Using TCGA database, higher METTL3 expression was found in CRC metastatic tissues and was associated with a poor prognosis. MeRIP-seq revealed that SRY (sex determining region Y)-box 2 (SOX2) was the downstream gene of METTL3. METTL3 knockdown in CRC cells drastically inhibited cell self-renewal, stem cell frequency and migration in vitro and suppressed CRC tumorigenesis and metastasis in both cell-based models and PDX models. Mechanistically, methylated SOX2 transcripts, specifically the coding sequence (CDS) regions, were subsequently recognized by the specific m6A “reader”, insulin-like growth factor 2 mRNA binding protein 2 (IGF2BP2), to prevent SOX2 mRNA degradation. Further, SOX2 expression positively correlated with METTL3 and IGF2BP2 in CRC tissues. The combined IHC panel, including “writer”, “reader”, and “target”, exhibited a better prognostic value for CRC patients than any of these components individually. Conclusions Overall, our study revealed that METTL3, acting as an oncogene, maintained SOX2 expression through an m6A-IGF2BP2-dependent mechanism in CRC cells, and indicated a potential biomarker panel for prognostic prediction in CRC. Electronic supplementary material The online version of this article (10.1186/s12943-019-1038-7) contains supplementary material, which is available to authorized users.
          Article 0 comments Cited 384 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Common variation at 6q16 within HACE1 and LIN28B influences susceptibility to neuroblastoma

            Sharon J. Diskin, Mario Capasso, Robert Schnepp … (2012)
            Neuroblastoma is a cancer of the sympathetic nervous system that accounts for approximately 10% of all pediatric oncology deaths 1 . Here we report on a genome-wide association study of 2,817 neuroblastoma cases and 7,473 controls. We identified two new associations at 6q16, the first within HACE1 (rs4336470; combined P = 2.7 × 10−11, odds ratio 1.26, 95% CI: 1.18–1.35) and the second within LIN28B (rs17065417; combined P = 1.2 × 10−8, odds ratio 1.38, 95% CI: 1.23–1.54). Expression of LIN28B and let-7 miRNA correlated with rs17065417 genotype in neuroblastoma cell lines, and we observed significant growth inhibition upon depletion of LIN28B specifically in neuroblastoma cells homozygous for the risk allele. Low HACE1 and high LIN28B expression in diagnostic primary neuroblastomas were associated with worse overall survival (P = 0.008 and 0.014, respectively). Taken together, we show that common variants in HACE1 and LIN28B influence neuroblastoma susceptibility and that both genes likely play a role in disease progression.
            Article 0 comments Cited 124 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Polymorphisms in the XPG gene and risk of gastric cancer in Chinese populations.

              Rui-Xi Hua, Ping Yu, Meng Wang … (2012)
              DNA repair genes play an important role in maintaining stability and integrity of genomic DNA. Polymorphisms in nucleotide excision repair genes may cause variations in DNA repair capacity phenotype and thus contribute to cancer risk. In this case-control study of 1,125 gastric cancer cases and 1,196 cancer-free controls, we investigated the association between three functional single nucleotide polymorphisms (SNPs, rs2296147T > C, rs2094258C > T and rs873601G > A) in the xeroderma pigmentosum group G (XPG) gene and gastric cancer risk. We used the Taqman assays to genotype these three SNPs and logistic regression models to estimate odds ratios (ORs) and 95% confidence intervals (95% CIs). We found that only the rs873601A variant genotypes were associated with a significant higher risk for gastric adenocarcinoma (adjusted OR = 1.30, 95% CI = 1.03-1.64 for AA vs. GG and adjusted OR = 1.23, 95% CI = 1.01-1.49 for AA vs. GG/AG). Stratification analysis indicated that this risk was more pronounced in subgroups of older age (>59 years), males, ever-smokers, and patients with NGCA. All these were not found for the other two SNPs (rs2296147T > C and rs2094258C > T). We then performed expression analysis using gastric cancer adjacent normal tissues from 141 patients and found that the A variant allele was associated with non-significantly reduced expression of XPG mRNA (P(trend) = 0.107). Further analysis using mRNA expression data from the HapMap suggested that the A allele was associated with significantly reduced expression of XPG mRNA in normal cell lines for 45 Chinese (P(trend) = 0.003) as well as for 261 subjects with different ethnicities (P(trend) = 0.001). These support the hypothesis that functional XPG variants may contribute to the risk of gastric cancer. Larger studies with different ethnic populations are warranted to validate our findings.
              Article 0 comments Cited 106 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Contributors
                Jun Bian: blandbird@126.com
                Jing He:
                ORCID: https://orcid.org/0000-0002-1954-2892
                hejing198374@gmail.com
                Journal
                Journal ID (nlm-ta): J Cell Mol Med
                Journal ID (iso-abbrev): J. Cell. Mol. Med
                Journal ID (doi): 10.1111/(ISSN)1582-4934
                Journal ID (publisher-id): JCMM
                Title: Journal of Cellular and Molecular Medicine
                Publisher: John Wiley and Sons Inc. (Hoboken )
                ISSN (Print): 1582-1838
                ISSN (Electronic): 1582-4934
                Publication date (Electronic): 02 July 2020
                Publication date (Print): August 2020
                Volume: 24
                Issue: 16 ( doiID: 10.1111/jcmm.v24.16 )
                Pages: 9280-9286
                Affiliations
                [ 1 ] Department of General Surgery Xi'an Children’s Hospital Xi'an Jiaotong University Affiliated Children's Hospital Xi'an China
                [ 2 ] Department of Pediatric Surgery Guangzhou Institute of Pediatrics Guangdong Provincial Key Laboratory of Research in Structural Birth Defect Disease Guangzhou Women and Children’s Medical Center Guangzhou Medical University Guangzhou China
                [ 3 ] Department of Clinical Laboratory Biobank, Harbin Medical University Cancer Hospital Harbin China
                [ 4 ] Department of Pediatric Surgery Shengjing Hospital of China Medical University Shenyang China
                [ 5 ] Department of Pediatric Surgery The First Affiliated Hospital of Zhengzhou University Zhengzhou China
                [ 6 ] Department of Pediatric Surgery Hunan Children’s Hospital Changsha China
                [ 7 ] Department of Pediatric Surgery The Second Affiliated Hospital of Xi’an Jiaotong University Xi’an China
                [ 8 ] Department of Hematology The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical University Wenzhou China
                [ 9 ] Department of Pathology Children Hospital and Women Health Center of Shanxi Taiyuan China
                [ 10 ] Kunming Key Laboratory of Children Infection and Immunity, Yunnan Key Laboratory of Children’s Major Disease Research Yunnan Institute of Pediatrics Research Yunnan Medical Center for Pediatric Diseases Kunming Children’s Hospital Kunming China
                Author notes
                [*] [* ] Correspondence

                Jing He, Department of Pediatric Surgery, Guangzhou Institute of Pediatrics, Guangdong Provincial Key Laboratory of Research in Structural Birth Defect Disease, Guangzhou Women and Children’s Medical Center, Guangzhou Medical University, 9 Jinsui Road, Guangzhou 510623, Guangdong, China.

                Email: hejing198374@ 123456gmail.com

                Jun Bian, Department of General Surgery, Xi'an Children's Hospital, Xi'an Jiaotong University Affiliated Children's Hospital, 69 Xiju Court Lane, Xi'an 710003, Shaanxi, China

                Email: blandbird@ 123456126.com

                Author information
                https://orcid.org/0000-0002-0408-3101
                https://orcid.org/0000-0002-1954-2892
                Article
                Publisher ID: JCMM15576
                DOI: 10.1111/jcmm.15576
                PMC ID: 7417682
                PubMed ID: 32615646
                SO-VID: 47c9bde4-04af-4826-9573-fa1e051e7420
                Copyright © © 2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd
                License:

                This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 26 April 2020
                Date revision received : 04 June 2020
                Date accepted : 10 June 2020
                Page count
                Figures: 0, Tables: 3, Pages: 7, Words: 5793
                Funding
                Funded by: Natural Science Foundation of Guangdong Province , open-funder-registry 10.13039/501100003453;
                Award ID: 2019A1515010360
                Funded by: Guangdong Provincial Key Laboratory of Research in Structural Birth Defect Disease
                Award ID: 2019B030301004
                Categories
                Subject: Original Article
                Subject: Original Articles
                Custom metadata
                source-schema-version-number 2.0
                cover-date August 2020
                details-of-publishers-convertor Converter:WILEY_ML3GV2_TO_JATSPMC version:5.8.6 mode:remove_FC converted:11.08.2020

                ScienceOpen disciplines: Molecular medicine
                Keywords: case‐control study,mettl3,neuroblastoma,polymorphism,risk
                Data availability:
                ScienceOpen disciplines: Molecular medicine
                Keywords: case‐control study, mettl3, neuroblastoma, polymorphism, risk

                Comments

                Comment on this article

                scite_

                Similar content724

                See all similar

                Cited by16

                See all cited by

                Most referenced authors837

                See all reference authors