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nature portfolio permissions reprints swi/snf chromatin-remodeling complex privacy policy ctcf-boundary-attenuated aml cells advertising nature social media single-cell epigenomic data editing india mir-196b promotes apoptosis mir-10a activates lpo microrna-mediated gene silencing wild-type cells transplanted mir-196b directly targets mirna-196b underpinning leukemogenesis acute myeloid leukemia early heart development post-transcriptional gene regulation springerlink instant access permissions illumine sequencing core 29 november 2021 bmc mol biol inducing intestinal neoplasia cis-regulatory regions rna-seq data mir-196b promoter penn state college mll-rearranged leukaemia published maps cell growth arrest collinear wnt repression hox cluster mirnas active histone modifications issue learn regulate gene expression privacy increasing fas expression hottip−/− aml cells leukemogenesis remains elusive polarized regulatory landscape cultured limb cells vulval development mol cell biol large gene lists colorectal cancer cells hoxa9 transcription factor inferring transcription-factor

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         headline:A coordinated function of lncRNA HOTTIP and miRNA-196b underpinning leukemogenesis by targeting FAS signaling
         description:MicroRNAs (miRNAs) may modulate more than 60% of human coding genes and act as negative regulators, whereas long noncoding RNAs (lncRNAs) regulate gene expression on multiple levels by interacting with chromatin, functional proteins, and RNAs such as mRNAs and microRNAs. However, the crosstalk between HOTTIP lncRNA and miRNAs in leukemogenesis remains elusive. Using combined integrated analyses of global miRNA expression profiling and state-of-the-art genomic analyses of chromatin such as ChIRP-seq (HOTTIP binding in genomewide), ChIP-seq, and ATAC-seq, we found that some miRNA genes are directly controlled by HOTTIP. Specifically, the HOX cluster miRNAs (miR-196a, miR-196b, miR-10a, and miR-10b), located cis and trans, were most dramatically regulated and significantly decreased in HOTTIP−/− AML cells. HOTTIP bound to the miR-196b promoter and HOTTIP deletion reduced chromatin accessibility and enrichment of active histone modifications at HOX cluster-associated miRNAs in AML cells, whereas reactivation of HOTTIP restored miR gene expression and chromatin accessibility in the CTCF-boundary-attenuated AML cells. Inactivation of HOTTIP or miR-196b promotes apoptosis by altering the chromatin signature at the FAS promoter and increasing FAS expression. Transplantation of miR-196b knockdown MOLM13 cells in NSG mice increased overall survival of mice compared to wild-type cells transplanted into mice. Thus, HOTTIP remodels the chromatin architecture around miRNAs to promote their transcription and consequently represses tumor suppressors and promotes leukemogenesis.
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      headline:A coordinated function of lncRNA HOTTIP and miRNA-196b underpinning leukemogenesis by targeting FAS signaling
      description:MicroRNAs (miRNAs) may modulate more than 60% of human coding genes and act as negative regulators, whereas long noncoding RNAs (lncRNAs) regulate gene expression on multiple levels by interacting with chromatin, functional proteins, and RNAs such as mRNAs and microRNAs. However, the crosstalk between HOTTIP lncRNA and miRNAs in leukemogenesis remains elusive. Using combined integrated analyses of global miRNA expression profiling and state-of-the-art genomic analyses of chromatin such as ChIRP-seq (HOTTIP binding in genomewide), ChIP-seq, and ATAC-seq, we found that some miRNA genes are directly controlled by HOTTIP. Specifically, the HOX cluster miRNAs (miR-196a, miR-196b, miR-10a, and miR-10b), located cis and trans, were most dramatically regulated and significantly decreased in HOTTIP−/− AML cells. HOTTIP bound to the miR-196b promoter and HOTTIP deletion reduced chromatin accessibility and enrichment of active histone modifications at HOX cluster-associated miRNAs in AML cells, whereas reactivation of HOTTIP restored miR gene expression and chromatin accessibility in the CTCF-boundary-attenuated AML cells. Inactivation of HOTTIP or miR-196b promotes apoptosis by altering the chromatin signature at the FAS promoter and increasing FAS expression. Transplantation of miR-196b knockdown MOLM13 cells in NSG mice increased overall survival of mice compared to wild-type cells transplanted into mice. Thus, HOTTIP remodels the chromatin architecture around miRNAs to promote their transcription and consequently represses tumor suppressors and promotes leukemogenesis.
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      name:Department of Biochemistry and Molecular Biology, Pennsylvania State University College of Medicine, Hershey, USA
      name:Thoracic Surgery Branch, National Cancer Institute, National Institutes of Health, Bethesda, USA
      name:Division of Pediatric Hematology/Oncology, Department of Pediatrics, Pennsylvania State University College of Medicine, Hershey, USA
      name:Penn State Cancer Institute, Pennsylvania State University College of Medicine, Hershey, USA
      name:Division of Pediatric Hematology/Oncology, Department of Pediatrics, Pennsylvania State University College of Medicine, Hershey, USA
      name:Division of Pediatric Hematology/Oncology, Department of Pediatrics, Pennsylvania State University College of Medicine, Hershey, USA
      name:Division of Pediatric Hematology/Oncology, Department of Pediatrics, Pennsylvania State University College of Medicine, Hershey, USA
      name:Penn State Cancer Institute, Pennsylvania State University College of Medicine, Hershey, USA
      name:Division of Hematology and Oncology, Department of Medicine, Pennsylvania State University College of Medicine, Hershey, USA
      name:Department of Pharmacology, Pennsylvania State University College of Medicine, Hershey, USA
      name:Division of Pediatric Hematology/Oncology, Department of Pediatrics, Pennsylvania State University College of Medicine, Hershey, USA
      name:Division of Pediatric Hematology/Oncology, Department of Pediatrics, Pennsylvania State University College of Medicine, Hershey, USA
      name:Penn State Cancer Institute, Pennsylvania State University College of Medicine, Hershey, USA
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