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Topics {✒️}

modulating wnt/β-catenin/myc/hmgcs2 axis mettl14-mediated n6-methyladenosine modification mir-214-5p/cox20 signaling pathway full size image mettl16/rab11b-as1 regulatory axis ythdf2-dependent posttranscriptional silencing stably overexpressed rab11b-as1 h19-mediated metastasis suppression ji-hang yuan large-scale clip-seq data shu-han sun random high-power fields article download pdf mir-654-3p/akt3 axis m6a-dependent manner rna n6-methyladenosine methyltransferase activating p38-mapk signaling wilcoxon signed-rank test adenosine methyltransferase mettl14 protein–rna interaction networks ez-magna rip kit rab11b-as1 transcript level low s-adenosylmethionine condition kaplan–meier survival analysis liver hepatocellular carcinoma multiple comparisons test cdna encoding rab11b-as1 tgf-β promotes lncrna-hnf1a-as1 functions median rab11b-as1 level mammalian rna demethylase rab11b-as1 overexpression reversed rab11b-as1 overexpression plasmid rab11b-as1 concurrent overexpression identified lncrna rab11b-as1 sponging mir-30b-3p rab11b-as1 stable overexpression rab11b-as1 transcript stability rab11b-as1 expression levels full access reduced rab11b-as1 stability rab11b-as1 expression level hcc-related m6a methyltransferase rab11b-as1 overexpression formed terminal deoxynucleotidyl transferase lower rab11b-as1 level rab11b-as1 overexpression vector rab11b-as1 m6a modification 8-μm pore size silico tool encori

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WebPage:
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         headline:METTL16 promotes hepatocellular carcinoma progression through downregulating RAB11B-AS1 in an m6A-dependent manner
         description:The molecular mechanisms driving hepatocellular carcinoma (HCC) remain largely unclear. As one of the major epitranscriptomic modifications, N6-methyladenosine (m6A) plays key roles in HCC. The aim of this study was to investigate the expression, roles, and mechanisms of action of the RNA methyltransferase methyltransferase-like protein 16 (METTL16) in HCC. The expression of METTL16 and RAB11B-AS1 was determined by RT-qPCR. The regulation of RAB11B-AS1 by METTL16 was investigated by RNA immunoprecipitation (RIP), methylated RIP (MeRIP), and RNA stability assays. In vitro and in vivo gain- and loss-of-function assays were performed to investigate the roles of METTL16 and RAB11B-AS1. METTL16 was upregulated in HCC, and its increased expression was correlated with poor prognosis of HCC patients. METTL16 promoted HCC cellular proliferation, migration, and invasion, repressed HCC cellular apoptosis, and promoted HCC tumoral growth in vivo. METTL16 directly bound long noncoding RNA (lncRNA) RAB11B-AS1, induced m6A modification of RAB11B-AS1, and decreased the stability of RAB11B-AS1 transcript, leading to the downregulation of RAB11B-AS1. Conversely to METTL16, RAB11B-AS1 is downregulated in HCC, and its decreased expression was correlated with poor prognosis of patients with HCC. Furthermore, the expression of RAB11B-AS1 was negatively correlated with METTL16 in HCC tissues. RAB11B-AS1 repressed HCC cellular proliferation, migration, and invasion, promoted HCC cellular apoptosis, and inhibited HCC tumoral growth in vivo. Functional rescue assays revealed that overexpression of RAB11B-AS1 reversed the oncogenic roles of METTL16 in HCC. This study identified the METTL16/RAB11B-AS1 regulatory axis in HCC, which represented novel targets for HCC prognosis and treatment.
         datePublished:2022-05-20T00:00:00Z
         dateModified:2022-05-20T00:00:00Z
         pageStart:1
         pageEnd:20
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         keywords:
            Hepatocellular carcinoma
             N 6-methyladenosine
            RNA methyltransferase
            Long noncoding RNA
            Tumor progression
            Cell Biology
            Biochemistry
            general
            Biological and Medical Physics
            Biophysics
            Biotechnology
            Molecular Medicine
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      headline:METTL16 promotes hepatocellular carcinoma progression through downregulating RAB11B-AS1 in an m6A-dependent manner
      description:The molecular mechanisms driving hepatocellular carcinoma (HCC) remain largely unclear. As one of the major epitranscriptomic modifications, N6-methyladenosine (m6A) plays key roles in HCC. The aim of this study was to investigate the expression, roles, and mechanisms of action of the RNA methyltransferase methyltransferase-like protein 16 (METTL16) in HCC. The expression of METTL16 and RAB11B-AS1 was determined by RT-qPCR. The regulation of RAB11B-AS1 by METTL16 was investigated by RNA immunoprecipitation (RIP), methylated RIP (MeRIP), and RNA stability assays. In vitro and in vivo gain- and loss-of-function assays were performed to investigate the roles of METTL16 and RAB11B-AS1. METTL16 was upregulated in HCC, and its increased expression was correlated with poor prognosis of HCC patients. METTL16 promoted HCC cellular proliferation, migration, and invasion, repressed HCC cellular apoptosis, and promoted HCC tumoral growth in vivo. METTL16 directly bound long noncoding RNA (lncRNA) RAB11B-AS1, induced m6A modification of RAB11B-AS1, and decreased the stability of RAB11B-AS1 transcript, leading to the downregulation of RAB11B-AS1. Conversely to METTL16, RAB11B-AS1 is downregulated in HCC, and its decreased expression was correlated with poor prognosis of patients with HCC. Furthermore, the expression of RAB11B-AS1 was negatively correlated with METTL16 in HCC tissues. RAB11B-AS1 repressed HCC cellular proliferation, migration, and invasion, promoted HCC cellular apoptosis, and inhibited HCC tumoral growth in vivo. Functional rescue assays revealed that overexpression of RAB11B-AS1 reversed the oncogenic roles of METTL16 in HCC. This study identified the METTL16/RAB11B-AS1 regulatory axis in HCC, which represented novel targets for HCC prognosis and treatment.
      datePublished:2022-05-20T00:00:00Z
      dateModified:2022-05-20T00:00:00Z
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      pageEnd:20
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      sameAs:https://doi.org/10.1186/s11658-022-00342-8
      keywords:
         Hepatocellular carcinoma
          N 6-methyladenosine
         RNA methyltransferase
         Long noncoding RNA
         Tumor progression
         Cell Biology
         Biochemistry
         general
         Biological and Medical Physics
         Biophysics
         Biotechnology
         Molecular Medicine
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      name:Department of Medical Genetics, Naval Medical University, Shanghai, China
      name:Department of Medical Genetics, Naval Medical University, Shanghai, China
      name:Department of Medical Genetics, Naval Medical University, Shanghai, China
      name:Department of Interventional Radiology, Changhai Hospital, Naval Medical University, Shanghai, China
      name:Department of Medical Genetics, Naval Medical University, Shanghai, China
      name:Department of Medical Genetics, Naval Medical University, Shanghai, China

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