We are analyzing https://link.springer.com/article/10.1186/s12943-018-0847-4.

Title:
Novel insights on m6A RNA methylation in tumorigenesis: a double-edged sword | Molecular Cancer
Description:
N6-methyladenosine (m6A), the most prevalent modification of mammalian RNA, has received increasing attention. Although m6A has been shown to be associated with biological activities, such as spermatogenesis modulation, cell spermatogenesis and pluripotency, Drosophila sex determination, and the control of T cell homeostasis and response to heat shock, little is known about its roles in cancer biology and cancer stem cells. Recent articles have noted that some genes have abnormal m6A expression after tumorigenesis, including genes ABS2, RARA, MYB, MYC, ADAM19 and FOX1. Abnormal changes in the m6A levels of these genes are closely related to tumour occurrence and development. In this review, we summarized the ‘dual edge weapon’ role of RNA methylation in the tumorigenesis. We discussed RNA methylation could lead to not only tumour progression but also tumour suppression. Moreover, we clarified that the abnormal changes in the m6A enrichment of specific loci contribute to tumour occurrence and development, thereby representing a novel anti-cancer strategy by restoration to balanced RNA methylation in tumour cells.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

Education
Science
Health & Fitness

Content Management System {📝}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month

Based on our best estimate, this website will receive around 5,000,019 visitors per month in the current month.
However, some sources were not loaded, we suggest to reload the page to get complete results.

check SE Ranking
check Ahrefs
check Similarweb
check Ubersuggest
check Semrush

How Does Link.springer.com Make Money? {💸}

We can't figure out the monetization strategy.

While profit motivates many websites, others exist to inspire, entertain, or provide valuable resources. Websites have a variety of goals. And this might be one of them. Link.springer.com might be making money, but it's not detectable how they're doing it.

Keywords {🔍}

pubmed, article, google, scholar, cas, cancer, rna, modification, cell, mettl, levels, mrna, methylation, central, tumour, modifications, protein, cells, expression, aberrant, tumorigenesis, wang, nmethyladenosine, stem, development, role, ultimately, methyltransferase, lung, fto, suppressor, breast, translation, leads, gene, carcinoma, socs, high, glioblastoma, molecular, genes, aml, zhang, chen, nature, occurrence, proteins, important, decreased, hcc,

Topics {✒️}

s-adenosyl methionine-binding protein sex-determining gene sex-lethal post-transcriptional chemical modifications article download pdf zinc finger ccch-type methyl-substituted nucleoside constituents n6-methyladenosine rna methylation n6-methyladenosine-dependent regulation conserved m6a-binding pocket a-dependent translation control dna methylation-based prognosis mir-33a suppresses proliferation downstream signal il-7/stat5 il-7/stat5/socs pathways full access tumour-specific mrna behaviour mettl3−/mettl14-mediated mrna mrna n6-adenosine methyltransferase regulated protein-rna interactome small-cell lung carcinoma drosophila sex determination modulates m6a deposition drosophila include inducer early-stage breast cancer methionine adenosyltransferase 2a mrna methylation controls m6a-based modifications occur inhibiting tumor suppressor decreased rna methylation scientific research program isolated mammalian rna mammalian rna demethylase double-edged sword privacy choices/manage cookies adomet-binding subunit promote tumour growth rna methyltransferase complex obvious physiological abnormality messenger rna stability abundant rna modifications rna methylation regulates acute myeloid leukaemia m6a rna methylation renbing jia small molecular inhibitor discussed rna methylation balanced rna methylation rna methylation triggers histone methyltransferases ezh2 sex determining region

Schema {🗺️}

WebPage:
      mainEntity:
         headline:Novel insights on m6A RNA methylation in tumorigenesis: a double-edged sword
         description:N6-methyladenosine (m6A), the most prevalent modification of mammalian RNA, has received increasing attention. Although m6A has been shown to be associated with biological activities, such as spermatogenesis modulation, cell spermatogenesis and pluripotency, Drosophila sex determination, and the control of T cell homeostasis and response to heat shock, little is known about its roles in cancer biology and cancer stem cells. Recent articles have noted that some genes have abnormal m6A expression after tumorigenesis, including genes ABS2, RARA, MYB, MYC, ADAM19 and FOX1. Abnormal changes in the m6A levels of these genes are closely related to tumour occurrence and development. In this review, we summarized the ‘dual edge weapon’ role of RNA methylation in the tumorigenesis. We discussed RNA methylation could lead to not only tumour progression but also tumour suppression. Moreover, we clarified that the abnormal changes in the m6A enrichment of specific loci contribute to tumour occurrence and development, thereby representing a novel anti-cancer strategy by restoration to balanced RNA methylation in tumour cells.
         datePublished:2018-07-21T00:00:00Z
         dateModified:2018-07-21T00:00:00Z
         pageStart:1
         pageEnd:10
         license:http://creativecommons.org/publicdomain/zero/1.0/
         sameAs:https://doi.org/10.1186/s12943-018-0847-4
         keywords:
            RNA methylation
            m6A
            Tumorigenesis
            Cancer Research
            Oncology
         image:
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fs12943-018-0847-4/MediaObjects/12943_2018_847_Fig1_HTML.png
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fs12943-018-0847-4/MediaObjects/12943_2018_847_Fig2_HTML.png
         isPartOf:
            name:Molecular Cancer
            issn:
               1476-4598
            volumeNumber:17
            type:
               Periodical
               PublicationVolume
         publisher:
            name:BioMed Central
            logo:
               url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
               type:ImageObject
            type:Organization
         author:
               name:Shaoyun Wang
               affiliation:
                     name:Shanghai Jiao Tong University School of Medicine
                     address:
                        name:Department of Ophthalmology, Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People’s Republic of China
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Peiwei Chai
               affiliation:
                     name:Shanghai Jiao Tong University School of Medicine
                     address:
                        name:Department of Ophthalmology, Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People’s Republic of China
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Ruobing Jia
               affiliation:
                     name:Shanghai Jiao Tong University School of Medicine
                     address:
                        name:Department of Ophthalmology, Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People’s Republic of China
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Renbing Jia
               affiliation:
                     name:Shanghai Jiao Tong University School of Medicine
                     address:
                        name:Department of Ophthalmology, Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People’s Republic of China
                        type:PostalAddress
                     type:Organization
               email:[email protected]
               type:Person
         isAccessibleForFree:1
         type:ScholarlyArticle
      context:https://schema.org
ScholarlyArticle:
      headline:Novel insights on m6A RNA methylation in tumorigenesis: a double-edged sword
      description:N6-methyladenosine (m6A), the most prevalent modification of mammalian RNA, has received increasing attention. Although m6A has been shown to be associated with biological activities, such as spermatogenesis modulation, cell spermatogenesis and pluripotency, Drosophila sex determination, and the control of T cell homeostasis and response to heat shock, little is known about its roles in cancer biology and cancer stem cells. Recent articles have noted that some genes have abnormal m6A expression after tumorigenesis, including genes ABS2, RARA, MYB, MYC, ADAM19 and FOX1. Abnormal changes in the m6A levels of these genes are closely related to tumour occurrence and development. In this review, we summarized the ‘dual edge weapon’ role of RNA methylation in the tumorigenesis. We discussed RNA methylation could lead to not only tumour progression but also tumour suppression. Moreover, we clarified that the abnormal changes in the m6A enrichment of specific loci contribute to tumour occurrence and development, thereby representing a novel anti-cancer strategy by restoration to balanced RNA methylation in tumour cells.
      datePublished:2018-07-21T00:00:00Z
      dateModified:2018-07-21T00:00:00Z
      pageStart:1
      pageEnd:10
      license:http://creativecommons.org/publicdomain/zero/1.0/
      sameAs:https://doi.org/10.1186/s12943-018-0847-4
      keywords:
         RNA methylation
         m6A
         Tumorigenesis
         Cancer Research
         Oncology
      image:
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fs12943-018-0847-4/MediaObjects/12943_2018_847_Fig1_HTML.png
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fs12943-018-0847-4/MediaObjects/12943_2018_847_Fig2_HTML.png
      isPartOf:
         name:Molecular Cancer
         issn:
            1476-4598
         volumeNumber:17
         type:
            Periodical
            PublicationVolume
      publisher:
         name:BioMed Central
         logo:
            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
         type:Organization
      author:
            name:Shaoyun Wang
            affiliation:
                  name:Shanghai Jiao Tong University School of Medicine
                  address:
                     name:Department of Ophthalmology, Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People’s Republic of China
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Peiwei Chai
            affiliation:
                  name:Shanghai Jiao Tong University School of Medicine
                  address:
                     name:Department of Ophthalmology, Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People’s Republic of China
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Ruobing Jia
            affiliation:
                  name:Shanghai Jiao Tong University School of Medicine
                  address:
                     name:Department of Ophthalmology, Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People’s Republic of China
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Renbing Jia
            affiliation:
                  name:Shanghai Jiao Tong University School of Medicine
                  address:
                     name:Department of Ophthalmology, Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People’s Republic of China
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
      isAccessibleForFree:1
["Periodical","PublicationVolume"]:
      name:Molecular Cancer
      issn:
         1476-4598
      volumeNumber:17
Organization:
      name:BioMed Central
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:Shanghai Jiao Tong University School of Medicine
      address:
         name:Department of Ophthalmology, Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People’s Republic of China
         type:PostalAddress
      name:Shanghai Jiao Tong University School of Medicine
      address:
         name:Department of Ophthalmology, Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People’s Republic of China
         type:PostalAddress
      name:Shanghai Jiao Tong University School of Medicine
      address:
         name:Department of Ophthalmology, Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People’s Republic of China
         type:PostalAddress
      name:Shanghai Jiao Tong University School of Medicine
      address:
         name:Department of Ophthalmology, Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People’s Republic of China
         type:PostalAddress
ImageObject:
      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:Shaoyun Wang
      affiliation:
            name:Shanghai Jiao Tong University School of Medicine
            address:
               name:Department of Ophthalmology, Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People’s Republic of China
               type:PostalAddress
            type:Organization
      name:Peiwei Chai
      affiliation:
            name:Shanghai Jiao Tong University School of Medicine
            address:
               name:Department of Ophthalmology, Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People’s Republic of China
               type:PostalAddress
            type:Organization
      name:Ruobing Jia
      affiliation:
            name:Shanghai Jiao Tong University School of Medicine
            address:
               name:Department of Ophthalmology, Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People’s Republic of China
               type:PostalAddress
            type:Organization
      name:Renbing Jia
      affiliation:
            name:Shanghai Jiao Tong University School of Medicine
            address:
               name:Department of Ophthalmology, Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People’s Republic of China
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Department of Ophthalmology, Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People’s Republic of China
      name:Department of Ophthalmology, Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People’s Republic of China
      name:Department of Ophthalmology, Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People’s Republic of China
      name:Department of Ophthalmology, Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People’s Republic of China

External Links {🔗}(299)

Analytics and Tracking {📊}

Google Tag Manager

Libraries {📚}

Clipboard.js
Prism.js

CDN Services {📦}

Crossref

4.7s.

LINK . SPRINGER . COM {}