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.
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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

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WebPage:
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         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
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            Breast cancer
            Prognosis
            Migration; transcription
            Cancer Research
            Oncology
            Surgical Oncology
            Health Promotion and Disease Prevention
            Biomedicine
            general
            Medicine/Public Health
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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.
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      dateModified:2019-04-05T00:00:00Z
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         N6-methyladenosine
         Breast cancer
         Prognosis
         Migration; transcription
         Cancer Research
         Oncology
         Surgical Oncology
         Health Promotion and Disease Prevention
         Biomedicine
         general
         Medicine/Public Health
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            address:
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               type:PostalAddress
            type:Organization
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      affiliation:
            name:Harbin Medical University Cancer Hospital
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               type:PostalAddress
            type:Organization
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      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

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