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MIR10B (microRNA 10b)

Written2008-06Begum Akman, Ayse Elif Erson
Department of Biology, Office 141, Laboratory, B-56, Middle East Technical University, Ankara 06531, Turkey

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Alias (NCBI)MIRN10B (microRNA 10b)
HGNC (Hugo) MIR10B
HGNC Alias symbhsa-mir-10b
HGNC Previous nameMIRN10B
LocusID (NCBI) 406903
Atlas_Id 44292
Location 2q31.1  [Link to chromosome band 2q31]
Location_base_pair Starts at 176150303 and ends at 176150412 bp from pter ( according to GRCh38/hg38-Dec_2013)  [Mapping MIR10B.png]
Local_order Based on Mapviewer Genes on Sequence, genes flanking MIRN10B oriented from centromere to telomere on 2q31.1 are:
HOXD11; Homeobox 11, 2q31.1
HOXD 10; Homeobox 10, 2q31.1
HOXD 9; Homeobox 9, 2q31.1
HOXD 8; Homeobox 8, 2q31.1
MIRN10B; microRNA 10b, 2q31.1
HOXD 4; Homeobox 4, 2q31.1
HOXD 3; Homeobox3, 2q31.1
MTX2; Metaxin 2, 2q31.1
Fusion genes
(updated 2017)
Data from Atlas, Mitelman, Cosmic Fusion, Fusion Cancer, TCGA fusion databases with official HUGO symbols (see references in chromosomal bands)


  Stem-loop structure of mir-10b.
Description In human, microRNA-10 gene has been duplicated. It is now present in the form of two variants as miR-10a and miR-10b located on different chromosomes. miR-10a is located between HOX4B and HOX5B on 17q21, while miR-10b is located between HOXD4 and HOXD8 on 2q31.1. It is believed that, there is a strong correlation between the specific miRs and HOX genes. MIRN10B maps to the HOXD cluster on 2q31.1. HOX genes are a family of transcription factor genes that play crucial roles during normal development and in oncogenesis. HOXD4 expression is deregulated in a variety of solid and hematopoietic cancers.
Transcription miRNAs are generally transcribed by RNA polymerase II.
There is limited information on how miRNA gene expression is regulated due to lack of basic information of their gene structures. Screening of miRNA putative promoter regions (miPPRs) revealed miPPR-10b for MIRN10B. TWIST1, a metastasis-promoting transcription factor, has been shown to induce miR-10b via binding to the most proximal E-box upstream of the miR-10b hairpin region. This E-box was in the miPPR-10b.
Pri-miRNA (primary) mir-10b: The primary miRNA transcripts are called pri-miRNAs. They contain cap structures and poly(A) tails. If transcribed by RNA polymerase II, primary transcript of mir-10b is not known yet.
  • Pre-miRNA (precursor) mir-10b: pri-miRNA transcripts are processed by microprocessor complex consisting nuclear RNase enzyme Drosha and the double-stranded RNA binding protein Pasha to generate pre-miRNAs. The precursor mir-10b is 110 nucleotides long. Pre-miR-10b is transferred from nucleus to cytoplasm.
  • Mature miR-10b: In the cytoplasm, pre-miRNA molecules are processed into mature miRNA by RNA-induced silencing complex (RISC). Mature miR-10b is 23 nucleotides long.
  • Pseudogene No reported pseudogenes.


    Note microRNAs are not translated into amino acids.


    Note Gene mutations have not been described.

    Implicated in

    Entity Colorectal neoplasia
    Disease Possible changes in microRNA levels; including miR-10b, was investigated during colorectal tumorigenesis. There was not a significant down-regulation of microRNA 10b in colon tumors to suggest a potential role in colorectal tumorigenesis.
    Entity Breast Cancer
    Disease 76 breast cancers and 10 normal breast samples were analyzed by microRNA microarray and Northern Blotting to identify miRNAs whose expression is deregulated notably in cancer versus normal breast tissues. According to these results; miR-10b was one of the microRNAs which were down-regulated.
    Regulation and function of miR-10b in breast cancer metastasis.
    Oncogenesis Tumor invasion and Metastasis: Although miR-10b was downregulated in nonmetastatic breast cancers in comparison with normal breast tissue, this miRNA was over-expressed in about 50% of metastatic breast cancers. Ectopic expression of miR-10b had no effect on proliferation, but an increase in transwell migration and Matrigel invasion was observed. In vivo ectopic expression of miR-10b conferred invasive properties on otherwise non-invasive breast cancer cells. Although control tumors could not invade surrounding tissues and exhibited poor vascularization, miR-10b over-expressing tumors exhibited an invasive behavior and were highly vascularized. miR-10b promoted metastasis in non-metastatic breast cancer cells. Lung micro-metastasis was detected in miR-10b over-expressing cells while there were no intravasating cells or lung metastases in control tumors.
    It was shown that miR-10b expression was induced by transcription factor TWIST allowing miR-10b to inhibit translation of the mRNA encoding homeobox D10 (Figure 2). This resulted in increased expression of a well-characterized prometastatic gene, RHOC (ras homolog gene family member C), thus leading to migration, tumor invasion, and metastasis.
    Entity Glioblastoma
    Disease miR-10b was one of the over-expressed miRNAs in glioblastomas compared to peripheral tissues. According to the microarray studies on glioblastomas, an excess of 1.97- to 13.6-fold increase was observed in 5 in out of 9 samples. This data was further confirmed by Northern blotting. miR-10b was stated to be a candidate oncogene microRNA as it was significantly upregulated in glioblastomas.
    Entity Acute Myeloid Leukemia (AML)
    Disease Role of microRNAs in the biology of NPMc+ (nucleophosmin) AML was investigated in 85 adult de novo AML patients. Microarray studies characterized these patients for subcellular localization/mutation status of NPM1 and FLT3 mutations. A strong microRNA expression pattern was identified which differentiated NPMc+ mutated from the cytoplasmic-negative (NPM1 unmutated) cases. According to this pattern, miRNA-10b together with miRNA-10a, let-7 and miR-29 family members were up-regulated. These data was further confirmed by qRT-PCR in 44 AML patients (randomly chosen from the initial cohort). According to the overall results, it was remarkable that miRNA-10b and miRNA-10a expression levels clearly differentiated NPMc+ vs. NPMc- cases.
    Entity Central Nervous System (CNS) tumors
    Disease Although, miRNA-10b was not specifically expressed in brain tissue, it was one of the 5 microRNAs which were highly expressed in CNS tumor-derived cell lines compared to normal brain tissue.
    Entity Hepatocellular adenomas (HCAs) and Hepatocellular Carcinomas (HCCs)
    Disease Expression of miRNAs was analyzed in a series of 46 malignant and benign hepatocellular tumors compared to 4 normal liver tissues. The most significant deregulated miRNAs were further analyzed in a second series of 43 tumors and 16 non-tumor liver tissues including cirrhosis and chronic hepatitis of various etiologies. miRNA-10b was found to be overexpressed in HCC when compared to benign tumors and non-tumor liver tissues.
    Entity Protein synthesis inhibition
    Disease The apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like 3G (APOBEC3G or A3G) and other APOBEC family members were shown to induce protein synthesis by miRNAs such as miR-10b in 293T and HeLa cells. miRNA microarray results suggested overexpression of miR-10b in 293T cells. Luciferase assay showed A3G effects on miRNA mediated translational repression. A3G facilitates recruitment of miRNA-targeted mRNA to polysomes to synthesize more proteins and drives dissociation of miRNA-targeted mRNA from P-bodies.
    Entity Megakaryocytopoiesis
    Disease In order to discover regulatory pathways during megakaryocytic differentiation, microRNA expression profiling was performed for in vitro differentiated megakaryocytes derived from CD34+ hematopoietic progenitors. According to the PAM (predictive analysis of microarray), miR-10b was one of the microRNAs which were identified to be involved in megakaryocytic differentiation. Downregulation of miR-10b was shown by microarrays. But Northern blot analysis and q-RT-PCR results showed that miR-10a and miR-130a were the most significantly down-regulated among the examined miRNAs.
    Entity Adipogenesis
    Disease miR-10b was shown to be up-regulated during 3T3-L1 pre-adipocyte differentiation. It was stated that this up-regulation may not be related to an actual differentiation process and may be induced by growth arrest and/or hormonal stimulation.


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    This paper should be referenced as such :
    Akman, B ; Erson, AE
    MIR10B (microRNA 10b)
    Atlas Genet Cytogenet Oncol Haematol. 2009;13(5):360-363.
    Free journal version : [ pdf ]   [ DOI ]

    External links

    HGNC (Hugo)MIR10B   31498
    Entrez_Gene (NCBI)MIR10B    microRNA 10b
    AliasesMIRN10B; hsa-mir-10b; miRNA10B; mir-10b
    GeneCards (Weizmann)MIR10B
    Ensembl hg19 (Hinxton)ENSG00000207744 [Gene_View]
    Ensembl hg38 (Hinxton)ENSG00000207744 [Gene_View]  ENSG00000207744 [Sequence]  chr2:176150303-176150412 [Contig_View]  MIR10B [Vega]
    ICGC DataPortalENSG00000207744
    TCGA cBioPortalMIR10B
    AceView (NCBI)MIR10B
    Genatlas (Paris)MIR10B
    SOURCE (Princeton)MIR10B
    Genetics Home Reference (NIH)MIR10B
    Genomic and cartography
    GoldenPath hg38 (UCSC)MIR10B  -     chr2:176150303-176150412 +  2q31.1   [Description]    (hg38-Dec_2013)
    GoldenPath hg19 (UCSC)MIR10B  -     2q31.1   [Description]    (hg19-Feb_2009)
    GoldenPathMIR10B - 2q31.1 [CytoView hg19]  MIR10B - 2q31.1 [CytoView hg38]
    genome Data Viewer NCBIMIR10B [Mapview hg19]  
    Gene and transcription
    Genbank (Entrez)AJ550395 LM608341
    RefSeq transcript (Entrez)
    RefSeq genomic (Entrez)
    Consensus coding sequences : CCDS (NCBI)MIR10B
    Alternative Splicing GalleryENSG00000207744
    Gene ExpressionMIR10B [ NCBI-GEO ]   MIR10B [ EBI - ARRAY_EXPRESS ]   MIR10B [ SEEK ]   MIR10B [ MEM ]
    Gene Expression Viewer (FireBrowse)MIR10B [ Firebrowse - Broad ]
    GenevisibleExpression of MIR10B in : [tissues]  [cell-lines]  [cancer]  [perturbations]  
    BioGPS (Tissue expression)406903
    GTEX Portal (Tissue expression)MIR10B
    Human Protein AtlasENSG00000207744-MIR10B [pathology]   [cell]   [tissue]
    Protein : pattern, domain, 3D structure
    Domain families : Pfam (Sanger)
    Domain families : Pfam (NCBI)
    Conserved Domain (NCBI)MIR10B
    Blocks (Seattle)MIR10B
    Human Protein Atlas [tissue]ENSG00000207744-MIR10B [tissue]
    Protein Interaction databases
    Ontologies - Pathways
    PubMed151 Pubmed reference(s) in Entrez
    GeneRIFsGene References Into Functions (Entrez)
    REVIEW articlesautomatic search in PubMed
    Last year publicationsautomatic search in PubMed

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