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We are analyzing https://link.springer.com/article/10.1186/s12943-017-0674-z.

Title:
Oct4 transcriptionally regulates the expression of long non-coding RNAs NEAT1 and MALAT1 to promote lung cancer progression | Molecular Cancer
Description:
Background Oct4, a key stemness transcription factor, is overexpressed in lung cancer. Here, we reveal a novel transcription regulation of long non-coding RNAs (lncRNAs) by Oct4. LncRNAs have emerged as important players in cancer progression. Methods Oct4 chromatin-immunoprecipitation (ChIP)-sequencing and several lncRNA databases with literature annotation were integrated to identify Oct4-regulated lncRNAs. Luciferase activity, qRT-PCR and ChIP-PCR assays were conducted to examine transcription regulation of lncRNAs by Oct4. Reconstitution experiments of Oct4 and downstream lncRNAs in cell proliferation, migration and invasion assays were performed to confirm the Oct4-lncRNAs signaling axes in promoting lung cancer cell growth and motility. The expression correlations between Oct4 and lncRNAs were investigated in 124 lung cancer patients using qRT-PCR analysis. The clinical significance of Oct4/lncRNAs signaling axes were further evaluated using multivariate Cox regression and Kaplan-Meier analyses. Results We confirmed that seven lncRNAs were upregulated by direct binding of Oct4. Among them, nuclear paraspeckle assembly transcript 1 (NEAT1), metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) and urothelial carcinoma-associated 1 (UCA1) were validated as Oct4 transcriptional targets through promoter or enhancer activation. We showed that lung cancer cells overexpressing NEAT1 or MALAT1 and the Oct4-silenced cells reconstituted with NEAT1 or MALAT1 promoted cell proliferation, migration and invasion. In addition, knockdown of NEAT1 or MALAT1 abolished Oct4-mediated lung cancer cell growth and motility. These cell-based results suggested that Oct4/NEAT1 or Oct4/MALAT1 axis promoted oncogenesis. Clinically, Oct4/NEAT1/MALAT1 co-overexpression was an independent factor for prediction of poor outcome in 124 lung cancer patients. Conclusions Our study reveals a novel mechanism by which Oct4 transcriptionally activates NEAT1 via promoter and MALAT1 via enhancer binding to promote cell proliferation and motility, and led to lung tumorigenesis and poor prognosis.
Website Age:
28 years and 1 months (reg. 1997-05-29).

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


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Keywords {πŸ”}

oct, cancer, malat, neat, cells, lung, expression, lncrnas, pubmed, cell, article, google, scholar, rna, fig, promoter, enhancer, noncoding, cas, binding, transcription, proliferation, analysis, long, migration, lncrna, invasion, patients, data, uca, assay, qrtpcr, central, results, study, oncogenic, table, tumor, regions, wang, vector, oligo, activity, assays, transcriptional, chipseq, regulation, gene, luciferase, downstream,

Topics {βœ’οΈ}

lsd1/corest/rest corepressor complexes chromatin-immunoprecipitation-polymerase chain reaction tgf-Ξ²-induced upregulation oct4/neat1/malat1 signaling axis chip-pcr/qrt-pcr analyses reveal mir-377-3p-e2f3 pathway inducing epithelial-mesenchymal transition realtime-glo viability assay tumor-sphere formation assay oct4-induced oncogenic effects article download pdf yi-ching wang mir-497-5p/igf1r axes epigenetically suppressing mir-129-5p house chip-seq dataset oct4-mediated oncogenic effects stably-transfected cell lines oct4-lncrnas signaling axes oct4/lncrnas signaling axes oct4-dependent lincrna expression transiently overexpressing neat1 oct4-mediated transcriptional regulation oct4 stably-overexpressed a549 anchorage-independent growth assay oct4-induced enhancer activity oct4-silenced cl1-0 cells oct4/neat1/malat1 high expression multivariate cox regression oct4-mediated high expression oct4-mediated malat1 upregulation purified chromatin-immunoprecipitated dna wnt regulatory axis oct4-mediated neat1 upregulation triple-negative breast cancer oct4-silenced a549 cells lung cancer progression promoted cell proliferation metastasis-related gene expressions previously performed chip-seq chip-seq binding signal genome-wide analysis brca1-deficient breast cancer results unbiased chip-seq oct4/malat1 transcriptional axes 1Β ml serum-free medium human lung adenocarcinoma cell stem cell oct4-overexpressed a549 cells full access oct4-silenced cells reconstituted

Schema {πŸ—ΊοΈ}

WebPage:
      mainEntity:
         headline:Oct4 transcriptionally regulates the expression of long non-coding RNAs NEAT1 and MALAT1 to promote lung cancer progression
         description:Oct4, a key stemness transcription factor, is overexpressed in lung cancer. Here, we reveal a novel transcription regulation of long non-coding RNAs (lncRNAs) by Oct4. LncRNAs have emerged as important players in cancer progression. Oct4 chromatin-immunoprecipitation (ChIP)-sequencing and several lncRNA databases with literature annotation were integrated to identify Oct4-regulated lncRNAs. Luciferase activity, qRT-PCR and ChIP-PCR assays were conducted to examine transcription regulation of lncRNAs by Oct4. Reconstitution experiments of Oct4 and downstream lncRNAs in cell proliferation, migration and invasion assays were performed to confirm the Oct4-lncRNAs signaling axes in promoting lung cancer cell growth and motility. The expression correlations between Oct4 and lncRNAs were investigated in 124 lung cancer patients using qRT-PCR analysis. The clinical significance of Oct4/lncRNAs signaling axes were further evaluated using multivariate Cox regression and Kaplan-Meier analyses. We confirmed that seven lncRNAs were upregulated by direct binding of Oct4. Among them, nuclear paraspeckle assembly transcript 1 (NEAT1), metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) and urothelial carcinoma-associated 1 (UCA1) were validated as Oct4 transcriptional targets through promoter or enhancer activation. We showed that lung cancer cells overexpressing NEAT1 or MALAT1 and the Oct4-silenced cells reconstituted with NEAT1 or MALAT1 promoted cell proliferation, migration and invasion. In addition, knockdown of NEAT1 or MALAT1 abolished Oct4-mediated lung cancer cell growth and motility. These cell-based results suggested that Oct4/NEAT1 or Oct4/MALAT1 axis promoted oncogenesis. Clinically, Oct4/NEAT1/MALAT1 co-overexpression was an independent factor for prediction of poor outcome in 124 lung cancer patients. Our study reveals a novel mechanism by which Oct4 transcriptionally activates NEAT1 via promoter and MALAT1 via enhancer binding to promote cell proliferation and motility, and led to lung tumorigenesis and poor prognosis.
         datePublished:2017-06-14T00:00:00Z
         dateModified:2017-06-14T00:00:00Z
         pageStart:1
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         license:http://creativecommons.org/publicdomain/zero/1.0/
         sameAs:https://doi.org/10.1186/s12943-017-0674-z
         keywords:
            Oct4
            lncRNA
             MALAT1
             NEAT1
            Transcription regulation
            Lung cancer
            Cancer Research
            Oncology
         image:
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                        name:Department of Pharmacology, College of Medicine, National Cheng Kung University, Tainan, Taiwan
                        type:PostalAddress
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               name:Che-Chung Lin
               affiliation:
                     name:College of Medicine, National Cheng Kung University
                     address:
                        name:Department of Pharmacology, College of Medicine, National Cheng Kung University, Tainan, Taiwan
                        type:PostalAddress
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                     name:National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University
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                        name:Division of Thoracic Surgery, Department of Surgery, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan
                        type:PostalAddress
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                     name:College of Medicine, National Cheng Kung University
                     address:
                        name:Department of Pharmacology, College of Medicine, National Cheng Kung University, Tainan, Taiwan
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ScholarlyArticle:
      headline:Oct4 transcriptionally regulates the expression of long non-coding RNAs NEAT1 and MALAT1 to promote lung cancer progression
      description:Oct4, a key stemness transcription factor, is overexpressed in lung cancer. Here, we reveal a novel transcription regulation of long non-coding RNAs (lncRNAs) by Oct4. LncRNAs have emerged as important players in cancer progression. Oct4 chromatin-immunoprecipitation (ChIP)-sequencing and several lncRNA databases with literature annotation were integrated to identify Oct4-regulated lncRNAs. Luciferase activity, qRT-PCR and ChIP-PCR assays were conducted to examine transcription regulation of lncRNAs by Oct4. Reconstitution experiments of Oct4 and downstream lncRNAs in cell proliferation, migration and invasion assays were performed to confirm the Oct4-lncRNAs signaling axes in promoting lung cancer cell growth and motility. The expression correlations between Oct4 and lncRNAs were investigated in 124 lung cancer patients using qRT-PCR analysis. The clinical significance of Oct4/lncRNAs signaling axes were further evaluated using multivariate Cox regression and Kaplan-Meier analyses. We confirmed that seven lncRNAs were upregulated by direct binding of Oct4. Among them, nuclear paraspeckle assembly transcript 1 (NEAT1), metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) and urothelial carcinoma-associated 1 (UCA1) were validated as Oct4 transcriptional targets through promoter or enhancer activation. We showed that lung cancer cells overexpressing NEAT1 or MALAT1 and the Oct4-silenced cells reconstituted with NEAT1 or MALAT1 promoted cell proliferation, migration and invasion. In addition, knockdown of NEAT1 or MALAT1 abolished Oct4-mediated lung cancer cell growth and motility. These cell-based results suggested that Oct4/NEAT1 or Oct4/MALAT1 axis promoted oncogenesis. Clinically, Oct4/NEAT1/MALAT1 co-overexpression was an independent factor for prediction of poor outcome in 124 lung cancer patients. Our study reveals a novel mechanism by which Oct4 transcriptionally activates NEAT1 via promoter and MALAT1 via enhancer binding to promote cell proliferation and motility, and led to lung tumorigenesis and poor prognosis.
      datePublished:2017-06-14T00:00:00Z
      dateModified:2017-06-14T00:00:00Z
      pageStart:1
      pageEnd:12
      license:http://creativecommons.org/publicdomain/zero/1.0/
      sameAs:https://doi.org/10.1186/s12943-017-0674-z
      keywords:
         Oct4
         lncRNA
          MALAT1
          NEAT1
         Transcription regulation
         Lung cancer
         Cancer Research
         Oncology
      image:
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fs12943-017-0674-z/MediaObjects/12943_2017_674_Fig1_HTML.gif
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                     type:PostalAddress
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                  name:College of Medicine, National Cheng Kung University
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                     name:Institute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan
                     type:PostalAddress
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            affiliation:
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                  address:
                     name:Department of Pharmacology, College of Medicine, National Cheng Kung University, Tainan, Taiwan
                     type:PostalAddress
                  type:Organization
                  name:College of Medicine, National Cheng Kung University
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                     name:Institute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan
                     type:PostalAddress
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                     name:Department of Pharmacology, College of Medicine, National Cheng Kung University, Tainan, Taiwan
                     type:PostalAddress
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                  name:College of Medicine, National Cheng Kung University
                  address:
                     name:Department of Pharmacology, College of Medicine, National Cheng Kung University, Tainan, Taiwan
                     type:PostalAddress
                  type:Organization
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            name:Wu-Wei Lai
            affiliation:
                  name:National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University
                  address:
                     name:Division of Thoracic Surgery, Department of Surgery, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan
                     type:PostalAddress
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            name:Yi-Ching Wang
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            affiliation:
                  name:College of Medicine, National Cheng Kung University
                  address:
                     name:Department of Pharmacology, College of Medicine, National Cheng Kung University, Tainan, Taiwan
                     type:PostalAddress
                  type:Organization
                  name:College of Medicine, National Cheng Kung University
                  address:
                     name:Institute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan
                     type:PostalAddress
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      name:National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University
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         name:Division of Thoracic Surgery, Department of Surgery, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan
         type:PostalAddress
      name:College of Medicine, National Cheng Kung University
      address:
         name:Department of Pharmacology, College of Medicine, National Cheng Kung University, Tainan, Taiwan
         type:PostalAddress
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      affiliation:
            name:College of Medicine, National Cheng Kung University
            address:
               name:Department of Pharmacology, College of Medicine, National Cheng Kung University, Tainan, Taiwan
               type:PostalAddress
            type:Organization
            name:College of Medicine, National Cheng Kung University
            address:
               name:Institute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan
               type:PostalAddress
            type:Organization
      name:Yen-An Tang
      affiliation:
            name:College of Medicine, National Cheng Kung University
            address:
               name:Department of Pharmacology, College of Medicine, National Cheng Kung University, Tainan, Taiwan
               type:PostalAddress
            type:Organization
            name:College of Medicine, National Cheng Kung University
            address:
               name:Institute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan
               type:PostalAddress
            type:Organization
      name:Ying-Hung Lu
      affiliation:
            name:College of Medicine, National Cheng Kung University
            address:
               name:Department of Pharmacology, College of Medicine, National Cheng Kung University, Tainan, Taiwan
               type:PostalAddress
            type:Organization
      name:Che-Chung Lin
      affiliation:
            name:College of Medicine, National Cheng Kung University
            address:
               name:Department of Pharmacology, College of Medicine, National Cheng Kung University, Tainan, Taiwan
               type:PostalAddress
            type:Organization
      name:Wu-Wei Lai
      affiliation:
            name:National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University
            address:
               name:Division of Thoracic Surgery, Department of Surgery, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan
               type:PostalAddress
            type:Organization
      name:Yi-Ching Wang
      url:http://orcid.org/0000-0002-7694-2067
      affiliation:
            name:College of Medicine, National Cheng Kung University
            address:
               name:Department of Pharmacology, College of Medicine, National Cheng Kung University, Tainan, Taiwan
               type:PostalAddress
            type:Organization
            name:College of Medicine, National Cheng Kung University
            address:
               name:Institute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Department of Pharmacology, College of Medicine, National Cheng Kung University, Tainan, Taiwan
      name:Institute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan
      name:Department of Pharmacology, College of Medicine, National Cheng Kung University, Tainan, Taiwan
      name:Institute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan
      name:Department of Pharmacology, College of Medicine, National Cheng Kung University, Tainan, Taiwan
      name:Department of Pharmacology, College of Medicine, National Cheng Kung University, Tainan, Taiwan
      name:Division of Thoracic Surgery, Department of Surgery, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan
      name:Department of Pharmacology, College of Medicine, National Cheng Kung University, Tainan, Taiwan
      name:Institute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan

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