We are analyzing https://link.springer.com/article/10.1186/s12885-019-5538-z.

Title:
Changes of N6-methyladenosine modulators promote breast cancer progression | BMC Cancer
Description:
Background Breast cancer (BC) displays striking genetic, epigenetic and phenotypic diversity. N6-methyladenosine (m6A) in mRNA has emerged as a crucial epitranscriptomic modification that controls cancer self-renewal and cell fate. However, the key enzymes of m6A expression and function in human breast carcinogenesis remain unclear. Methods The expression of m6A methylases (METTL3, METTL14 and WTAP) and demethylases (FTO and ALKBH5) were analyzed by using ONCOMINE and The Cancer Genome Atlas databases and in 36 pairs of BC and adjacent non-cancerous tissue. The level of m6A in BC patients was detected by ELISA, and the function of m6A was analyzed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, colony formation assay and transwell assay. The database of bc-GenExMiner v4.0, Kaplan-Meier Plotter and cBioPortal were queried for correlation, mutation and prognosis analysis of BC. Results The m6A methylases and demethylases were dysregulated in several major malignant tumors. Specifically, the expression of all m6A methylases was reduced in BC as compared with normal controls, but the demethylase ALKBH5 was induced in ONCOMINE databases and confirmed in clinical patients. METTL14 expression was positively correlated with METTL3 expression, and both showed high expression in normal breast-like and luminal-A and -B BC. Functionally, reducing m6A expression by overexpressing METTL14 and/or knockdown of ALKBH5 could inhibit breast cell viability, colony formation and cell migration. Furthermore, Kaplan-Meier, meta-analysis and univariate Cox assay showed that the expression of m6A members including METTL3, METTL14, WTAP and FTO but not their gene mutation and amplification, was tightly associated with cancer progression and poor survival. Conclusions Changes of m6A modulators reduced m6A may promote tumorigenesis and predict poor prognosis in BC.
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 7,626,182 visitors per month in the current month.

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.

Earning money isn't the goal of every website; some are designed to offer support or promote social causes. People have different reasons for creating websites. This might be one such reason. Link.springer.com might have a hidden revenue stream, but it's not something we can detect.

Keywords {🔍}

mettl, cancer, expression, article, breast, analysis, google, scholar, patients, mrna, alkbh, cells, cell, data, wtap, fto, rna, table, cas, methylation, enzymes, clinical, survival, prognostic, fig, bcgenexminer, gene, normal, zhang, level, methylases, tissue, univariate, cox, assay, database, andor, molecular, size, wang, nmethyladenosine, full, human, members, tumor, glioblastoma, mdamb, status, enzyme, progression,

Topics {✒️}

rna n6-methyladenosine methyltransferase transfected mda-mb-231 cells central nervous system mda-mb-231 cell line reversible rna methylation/demethylation dengying wu & donghong zhang mrna expression z-scores ultra-low attachment plates english language editing protein expression z-scores heat-map represents data methyladenosine rna demethylase breast cancer research n6-methyladenosine mettl14 breast cancer progression full access mammalian rna demethylase dunnett-tukey-kramer test a-dependent translation control article download pdf kaplan-meier plots comparing rna methylation landscape rna methylation regulates epi-transcriptome research dna methylation mda-mb-231 cells colony size calculation 8-μm pore size possess methylation activity privacy choices/manage cookies cell counting kit-8 pcdna3/flag-mettl14 plasmid published independent datasets georgia state university qrt-pcr amplification involved transcription search search human breast cancer n6-methyladenosine reduced cell viability inhibiting bc growth percent cell viability creative commons license misregulated mrna methylation breast cancer prognosis breast cancer cells short-hairpin rna impacts rna metabolism m6a mrna methylation human cancer tissues m6a demethylase contributed

Schema {🗺️}

WebPage:
      mainEntity:
         headline:Changes of N6-methyladenosine modulators promote breast cancer progression
         description:Breast cancer (BC) displays striking genetic, epigenetic and phenotypic diversity. N6-methyladenosine (m6A) in mRNA has emerged as a crucial epitranscriptomic modification that controls cancer self-renewal and cell fate. However, the key enzymes of m6A expression and function in human breast carcinogenesis remain unclear. The expression of m6A methylases (METTL3, METTL14 and WTAP) and demethylases (FTO and ALKBH5) were analyzed by using ONCOMINE and The Cancer Genome Atlas databases and in 36 pairs of BC and adjacent non-cancerous tissue. The level of m6A in BC patients was detected by ELISA, and the function of m6A was analyzed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, colony formation assay and transwell assay. The database of bc-GenExMiner v4.0, Kaplan-Meier Plotter and cBioPortal were queried for correlation, mutation and prognosis analysis of BC. The m6A methylases and demethylases were dysregulated in several major malignant tumors. Specifically, the expression of all m6A methylases was reduced in BC as compared with normal controls, but the demethylase ALKBH5 was induced in ONCOMINE databases and confirmed in clinical patients. METTL14 expression was positively correlated with METTL3 expression, and both showed high expression in normal breast-like and luminal-A and -B BC. Functionally, reducing m6A expression by overexpressing METTL14 and/or knockdown of ALKBH5 could inhibit breast cell viability, colony formation and cell migration. Furthermore, Kaplan-Meier, meta-analysis and univariate Cox assay showed that the expression of m6A members including METTL3, METTL14, WTAP and FTO but not their gene mutation and amplification, was tightly associated with cancer progression and poor survival. Changes of m6A modulators reduced m6A may promote tumorigenesis and predict poor prognosis in BC.
         datePublished:2019-04-05T00:00:00Z
         dateModified:2019-04-05T00:00:00Z
         pageStart:1
         pageEnd:12
         license:http://creativecommons.org/publicdomain/zero/1.0/
         sameAs:https://doi.org/10.1186/s12885-019-5538-z
         keywords:
            N6-methyladenosine
            Breast cancer
            Prognosis
            Migration; transcription
            Cancer Research
            Oncology
            Surgical Oncology
            Health Promotion and Disease Prevention
            Biomedicine
            general
            Medicine/Public Health
         image:
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fs12885-019-5538-z/MediaObjects/12885_2019_5538_Fig1_HTML.png
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fs12885-019-5538-z/MediaObjects/12885_2019_5538_Fig2_HTML.png
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fs12885-019-5538-z/MediaObjects/12885_2019_5538_Fig3_HTML.png
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fs12885-019-5538-z/MediaObjects/12885_2019_5538_Fig4_HTML.png
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fs12885-019-5538-z/MediaObjects/12885_2019_5538_Fig5_HTML.png
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fs12885-019-5538-z/MediaObjects/12885_2019_5538_Fig6_HTML.png
         isPartOf:
            name:BMC Cancer
            issn:
               1471-2407
            volumeNumber:19
            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:Lianpin Wu
               affiliation:
                     name:The Second Affiliated Hospital of Wenzhou Medical University
                     address:
                        name:Department of Cardiology, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, China
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Dengying Wu
               affiliation:
                     name:The Second Affiliated Hospital of Wenzhou Medical University
                     address:
                        name:Department of Cardiology, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, China
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Jinfeng Ning
               affiliation:
                     name:The Thoracic Department of Harbin Medical University Cancer Hospital
                     address:
                        name:The Thoracic Department of Harbin Medical University Cancer Hospital, Harbin, China
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Wei Liu
               affiliation:
                     name:Harbin Medical University Cancer Hospital
                     address:
                        name:The Fourth Department of Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, China
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Donghong Zhang
               affiliation:
                     name:The Second Affiliated Hospital of Wenzhou Medical University
                     address:
                        name:Department of Cardiology, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, China
                        type:PostalAddress
                     type:Organization
                     name:Georgia State University
                     address:
                        name:Center for Molecular and Translational Medicine, Georgia State University, Atlanta, USA
                        type:PostalAddress
                     type:Organization
               email:[email protected]
               type:Person
         isAccessibleForFree:1
         type:ScholarlyArticle
      context:https://schema.org
ScholarlyArticle:
      headline:Changes of N6-methyladenosine modulators promote breast cancer progression
      description:Breast cancer (BC) displays striking genetic, epigenetic and phenotypic diversity. N6-methyladenosine (m6A) in mRNA has emerged as a crucial epitranscriptomic modification that controls cancer self-renewal and cell fate. However, the key enzymes of m6A expression and function in human breast carcinogenesis remain unclear. The expression of m6A methylases (METTL3, METTL14 and WTAP) and demethylases (FTO and ALKBH5) were analyzed by using ONCOMINE and The Cancer Genome Atlas databases and in 36 pairs of BC and adjacent non-cancerous tissue. The level of m6A in BC patients was detected by ELISA, and the function of m6A was analyzed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, colony formation assay and transwell assay. The database of bc-GenExMiner v4.0, Kaplan-Meier Plotter and cBioPortal were queried for correlation, mutation and prognosis analysis of BC. The m6A methylases and demethylases were dysregulated in several major malignant tumors. Specifically, the expression of all m6A methylases was reduced in BC as compared with normal controls, but the demethylase ALKBH5 was induced in ONCOMINE databases and confirmed in clinical patients. METTL14 expression was positively correlated with METTL3 expression, and both showed high expression in normal breast-like and luminal-A and -B BC. Functionally, reducing m6A expression by overexpressing METTL14 and/or knockdown of ALKBH5 could inhibit breast cell viability, colony formation and cell migration. Furthermore, Kaplan-Meier, meta-analysis and univariate Cox assay showed that the expression of m6A members including METTL3, METTL14, WTAP and FTO but not their gene mutation and amplification, was tightly associated with cancer progression and poor survival. Changes of m6A modulators reduced m6A may promote tumorigenesis and predict poor prognosis in BC.
      datePublished:2019-04-05T00:00:00Z
      dateModified:2019-04-05T00:00:00Z
      pageStart:1
      pageEnd:12
      license:http://creativecommons.org/publicdomain/zero/1.0/
      sameAs:https://doi.org/10.1186/s12885-019-5538-z
      keywords:
         N6-methyladenosine
         Breast cancer
         Prognosis
         Migration; transcription
         Cancer Research
         Oncology
         Surgical Oncology
         Health Promotion and Disease Prevention
         Biomedicine
         general
         Medicine/Public Health
      image:
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fs12885-019-5538-z/MediaObjects/12885_2019_5538_Fig1_HTML.png
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fs12885-019-5538-z/MediaObjects/12885_2019_5538_Fig2_HTML.png
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fs12885-019-5538-z/MediaObjects/12885_2019_5538_Fig3_HTML.png
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fs12885-019-5538-z/MediaObjects/12885_2019_5538_Fig4_HTML.png
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fs12885-019-5538-z/MediaObjects/12885_2019_5538_Fig5_HTML.png
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fs12885-019-5538-z/MediaObjects/12885_2019_5538_Fig6_HTML.png
      isPartOf:
         name:BMC Cancer
         issn:
            1471-2407
         volumeNumber:19
         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:Lianpin Wu
            affiliation:
                  name:The Second Affiliated Hospital of Wenzhou Medical University
                  address:
                     name:Department of Cardiology, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, China
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Dengying Wu
            affiliation:
                  name:The Second Affiliated Hospital of Wenzhou Medical University
                  address:
                     name:Department of Cardiology, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, China
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Jinfeng Ning
            affiliation:
                  name:The Thoracic Department of Harbin Medical University Cancer Hospital
                  address:
                     name:The Thoracic Department of Harbin Medical University Cancer Hospital, Harbin, China
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Wei Liu
            affiliation:
                  name:Harbin Medical University Cancer Hospital
                  address:
                     name:The Fourth Department of Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, China
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Donghong Zhang
            affiliation:
                  name:The Second Affiliated Hospital of Wenzhou Medical University
                  address:
                     name:Department of Cardiology, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, China
                     type:PostalAddress
                  type:Organization
                  name:Georgia State University
                  address:
                     name:Center for Molecular and Translational Medicine, Georgia State University, Atlanta, USA
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
      isAccessibleForFree:1
["Periodical","PublicationVolume"]:
      name:BMC Cancer
      issn:
         1471-2407
      volumeNumber:19
Organization:
      name:BioMed Central
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:The Second Affiliated Hospital of Wenzhou Medical University
      address:
         name:Department of Cardiology, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, China
         type:PostalAddress
      name:The Second Affiliated Hospital of Wenzhou Medical University
      address:
         name:Department of Cardiology, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, China
         type:PostalAddress
      name:The Thoracic Department of Harbin Medical University Cancer Hospital
      address:
         name:The Thoracic Department of Harbin Medical University Cancer Hospital, Harbin, China
         type:PostalAddress
      name:Harbin Medical University Cancer Hospital
      address:
         name:The Fourth Department of Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, China
         type:PostalAddress
      name:The Second Affiliated Hospital of Wenzhou Medical University
      address:
         name:Department of Cardiology, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, China
         type:PostalAddress
      name:Georgia State University
      address:
         name:Center for Molecular and Translational Medicine, Georgia State University, Atlanta, USA
         type:PostalAddress
ImageObject:
      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:Lianpin Wu
      affiliation:
            name:The Second Affiliated Hospital of Wenzhou Medical University
            address:
               name:Department of Cardiology, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, China
               type:PostalAddress
            type:Organization
      name:Dengying Wu
      affiliation:
            name:The Second Affiliated Hospital of Wenzhou Medical University
            address:
               name:Department of Cardiology, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, China
               type:PostalAddress
            type:Organization
      name:Jinfeng Ning
      affiliation:
            name:The Thoracic Department of Harbin Medical University Cancer Hospital
            address:
               name:The Thoracic Department of Harbin Medical University Cancer Hospital, Harbin, China
               type:PostalAddress
            type:Organization
      name:Wei Liu
      affiliation:
            name:Harbin Medical University Cancer Hospital
            address:
               name:The Fourth Department of Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, China
               type:PostalAddress
            type:Organization
      name:Donghong Zhang
      affiliation:
            name:The Second Affiliated Hospital of Wenzhou Medical University
            address:
               name:Department of Cardiology, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, China
               type:PostalAddress
            type:Organization
            name:Georgia State University
            address:
               name:Center for Molecular and Translational Medicine, Georgia State University, Atlanta, USA
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Department of Cardiology, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, China
      name:Department of Cardiology, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, China
      name:The Thoracic Department of Harbin Medical University Cancer Hospital, Harbin, China
      name:The Fourth Department of Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, China
      name:Department of Cardiology, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, China
      name:Center for Molecular and Translational Medicine, Georgia State University, Atlanta, USA

External Links {🔗}(112)

Analytics and Tracking {📊}

Google Tag Manager

Libraries {📚}

Clipboard.js
Prism.js

CDN Services {📦}

Crossref

5.03s.

LINK . SPRINGER . COM {}