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MIR211 (microRNA 211)

Written2013-05Amir Avan, Mina Maftouh, Godefridus J Peters, Elisa Giovannetti
Department of Medical Oncology, VU University Medical Center, Amsterdam, De Boelelaan 1117, 1081 HV Amsterdam, The Netherlands (AA, MM, GJP, EG); Department of New Sciences, Technology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran (AA, MM)

(Note : for Links provided by Atlas : click)

Identity

Alias_namesMIRN211
Alias_symbol (synonym)hsa-mir-211
Other aliasmir-211
HGNC (Hugo) MIR211
LocusID (NCBI) 406993
Atlas_Id 50533
Location 15q13.3  [Link to chromosome band 15q13]
Location_base_pair Starts at 31065032 and ends at 31065141 bp from pter ( according to hg19-Feb_2009)  [Mapping MIR211.png]
Local_order Based on Mapviewer, gene flanking miR-211 oriented on 15q13 are:
- FAN1 (FANCD2/FANCI-associated nuclease 1); 15q13.2-q13.3
- MTMR10 (myotubularin related protein 10); 15q13.3
- miR-211 (microRNA 211); 15q13.3
- TRPM1 (transient receptor potential cation channel, subfamily M, member 1); 15q13.3
- LOC283710; 15q13.3.
Fusion genes
(updated 2017)
Data from Atlas, Mitelman, Cosmic Fusion, Fusion Cancer, TCGA fusion databases with official HUGO symbols (see references in chromosomal bands)

DNA/RNA

 
  Location of miR-211 in chromosome 15q13. This gene is located in the intron 6 of the TRPM1 gene within 31357235-31357344 bp. The mature miR-211 is 22 nucleotides long.
Description miR-211 is located in the intron 6 of TRPM1 gene at 15q13, which is transcribed by RNA polymerase II.
Transcription The primary transcript contains of 110 nucleotides (TCACCTGGCC ATGTGACTTG TGGGCTTCCC TTTGTCATCC TTCGCCTAGG GCTCTGAGCA GGGCAGGGAC AGCAAAGGGG TGCTCAGTTG TCACTTCCCA CAGCACGGAG) which is cleaved by the Drosha ribonuclease III enzyme into 2 products, hsa-miR-211-5p (26-47 bp) and hsa-miR-211-3p (63-83 bp). This miRNA is further cleaved by the cytoplasmic Dicer ribonuclease to the mature miR-211 sequence (5'-UUCCCUUUGUCAUCCUUCGCCU-3') with stem-loop shape. In general, the mature miRNA is incorporated into a RNA-induced silencing complex (RISC), that can target mRNA through imperfect base pairing, leading to translational inhibition or destabilization of the target mRNA.
Pseudogene No reported pseudogenes.

Protein

Note This miRNA is not translated into amino acids.

Mutations

Note No mutations have been reported, while single nucleotide variations (SNPs) include: rs141424579, rs187960998, rs34520022 and rs140017415.

Implicated in

Note
  
Entity Pancreatic cancer
Note Giovannetti and collaborators, recently identified miR-211 as a prognostic factor in resected pancreatic ductal adenocarcinoma (PDAC) patients using high-throughput microarray analysis of more than 1200 human miRNAs in PDAC patients classified in short-term overall survivors versus long-term survivors (Giovannetti et al., 2012). This study evaluated 26 PDAC patients with homogeneous clinicopathological characteristics that underwent resection with curative intent and were treated with standard gemcitabine adjuvant regimen. The miRNA microarray analysis was carried out in 19 samples that passed the RNA quality criterion, including 13 patients with short survival and 6 patients with long survival. These results illustrated that patients with low miR-211 expression according to median value had a significantly shorter median overall survival compared to patients with high miR-211 expression (OS, 14.8, 95%CI = 13.1-16.5, vs. 25.7 months, 95%CI = 16.2-35.1, log-rank-P = 0.004). Multivariate analysis revealed that low miR-211 expression was an independent factor of poor prognosis (hazard ratio 2.3, P = 0.03). The expression of this miRNA was also assessed by quantitative-PCR in an independent cohort of laser-microdissected PDACs from 60 resected patients treated with the same gemcitabine regimen, showing the significant association of miR-211 expression status with both OS and disease-free-survival (DFS).
  
  
Entity Colorectal cancer
Note miR-211 has been found to be expressed in colorectal cancer and a recent study showed that over-expression of miR-211 in the colorectal cancer cell line HCT-116 promotes cellular growth in vitro and in vivo by downregulating the expression level of the CHD5 tumor suppressor gene (Cai et al., 2012).
  
  
Entity Glioblastoma
Note Glioblastoma multiforme (GBM) is the most aggressive brain tumor with less than one year survival time. Thus, there is an urgent need to identify new predictive/prognostic biomarkers that can predict/manage the patients at earlier stages. A recent study showed that miRNA-211 is downregulated in GBM, which might be due to aberrant methylation-mediated epigenetic silencing of the miR-211 promoter. Asuthkar and collaborators showed that miR-211 has an inhibitory effect on glioma cell invasion and migration via suppression of MMP-9 and demethylation of miR-211 promoter-associated CpG islands, which results in insensitivity of some GBMs to radiation and chemotherapy (Asuthkar et al., 2012).
  
  
Entity Oral carcinoma
Note High expression of miR-211 has been shown to be associated with the advanced nodal metastasis, vascular invasion, and poor prognosis of oral carcinoma. Chang and colleagues demonstrated that enforced miR-211 expression significantly increased the proliferation, migration, and anchorage-independent colony formation of oral carcinoma cells, while it enhanced the tumorigenicity (Chang et al., 2008).
  
  
Entity Breast cancer
Note Expression of 455 miRNAs was evaluated in a highly bone metastatic MDA-MB-231 variant, compared to the parental MDA-MB-231 breast cancer cell line. 16 miRNAs (3.5%) were found to have >3-fold expression difference between the two cell types. This study showed that miRNA-211 inhibits TGF-β-induced IL-11 production by binding to its 3' UTR in bone metastatic breast cancer cells (Pollari et al., 2012).
  
  
Entity Melanoma
Note Several studies showed that miR-211 is downregulated in melanoma and has been found to act as a tumour suppressor. In particular, Xu and collaborators performed miRNA microarray expression in 52 formalin-fixed and paraffin-embedded specimens from different stages of melanomagenesis and 15 cell lines. They showed that expression of miR-211 was down-regulated in melanoma cells and melanoblasts compared to melanocytes, and upregulation of miR-211 could lead to suppression of tumor invasion in melanoma (Levy et al., 2010; Mazar et al., 2010; Xu et al,. 2012).
  
  
Entity Cervical cancer
Note In cervical cancer, miR-211 has been shown to be upregulated, while inhibition of this miRNA decreased the growth of Hela cells (Cheng et al., 2005).
  
  
Entity Stroke risk
Note Brain vascular leaking and inflammation has been reported as two important pathological processes of stroke. Angiopoietin-1 is a vascular strengthening factor which acts a protective factor for pathological vascular inflammation and leakage. The rs2507800 variant is located in the miR-211-binding site of angiopoietin-1, Cheng and colleagues evaluated the effect of the variant on angiopoietin-1 translation. They showed that the A allele of rs2507800 inhibited angiopoietin-1 translation by facilitating miR-211 binding. Furthermore they assessed the association of the variant with stroke in 438 stroke patients and 890 controls, and replicated in an independent population of 1791 stroke patients and 1843 controls. These results illustrated that the TT genotype (rs2507800) in the 3'-UTR of angiopoietin-1 could reduce the risk of stroke by interacting with miR-211 binding (Chen et al., 2010).
  
  
Entity Human retinal pigment epithelium
Note Wang and collaborators identified the critical role of miR-211 in maintaining epithelial barrier function and cell physiology in human retinal pigment epithelium. Moreover they found that miR-211 is one of the most highly expressed microRNAs in human retinal pigment epithelium. Expression of this miRNA was significantly lower in the NCI60 tumor cell line panel compared with 13 normal tissues (Wang et al., 2010).
  

To be noted

This study was partially supported by grants from Netherlands Organization for Scientific Research, VENI grant (Elisa Giovannetti), CCA Foundation 2012 (Elisa Giovannetti, Amir Avan, Godefridus J Peters), Iranian grant from Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran (Amir Avan), Italian Minister of Research, AIRC/Marie Curie International Fellowship (Elisa Giovannetti), PRIN-2009 (Elisa Giovannetti), and Istituto Toscano Tumori (Elisa Giovannetti).

Bibliography

Epigenetic regulation of miRNA-211 by MMP-9 governs glioma cell apoptosis, chemosensitivity and radiosensitivity.
Asuthkar S, Velpula KK, Chetty C, Gorantla B, Rao JS.
Oncotarget. 2012 Nov;3(11):1439-54.
PMID 23183822
 
MicroRNA-211 expression promotes colorectal cancer cell growth in vitro and in vivo by targeting tumor suppressor CHD5.
Cai C, Ashktorab H, Pang X, Zhao Y, Sha W, Liu Y, Gu X.
PLoS One. 2012;7(1):e29750. doi: 10.1371/journal.pone.0029750. Epub 2012 Jan 3.
PMID 22235338
 
Association between high miR-211 microRNA expression and the poor prognosis of oral carcinoma.
Chang KW, Liu CJ, Chu TH, Cheng HW, Hung PS, Hu WY, Lin SC.
J Dent Res. 2008 Nov;87(11):1063-8.
PMID 18946016
 
A functional variant in the 3'-UTR of angiopoietin-1 might reduce stroke risk by interfering with the binding efficiency of microRNA 211.
Chen J, Yang T, Yu H, Sun K, Shi Y, Song W, Bai Y, Wang X, Lou K, Song Y, Zhang Y, Hui R.
Hum Mol Genet. 2010 Jun 15;19(12):2524-33. doi: 10.1093/hmg/ddq131. Epub 2010 Apr 8.
PMID 20378606
 
Antisense inhibition of human miRNAs and indications for an involvement of miRNA in cell growth and apoptosis.
Cheng AM, Byrom MW, Shelton J, Ford LP.
Nucleic Acids Res. 2005 Mar 1;33(4):1290-7. Print 2005.
PMID 15741182
 
High-throughput microRNA (miRNAs) arrays unravel the prognostic role of MiR-211 in pancreatic cancer.
Giovannetti E, van der Velde A, Funel N, Vasile E, Perrone V, Leon LG, De Lio N, Avan A, Caponi S, Pollina LE, Galla V, Sudo H, Falcone A, Campani D, Boggi U, Peters GJ.
PLoS One. 2012;7(11):e49145. doi: 10.1371/journal.pone.0049145. Epub 2012 Nov 14.
PMID 23155457
 
Intronic miR-211 assumes the tumor suppressive function of its host gene in melanoma.
Levy C, Khaled M, Iliopoulos D, Janas MM, Schubert S, Pinner S, Chen PH, Li S, Fletcher AL, Yokoyama S, Scott KL, Garraway LA, Song JS, Granter SR, Turley SJ, Fisher DE, Novina CD.
Mol Cell. 2010 Dec 10;40(5):841-9. doi: 10.1016/j.molcel.2010.11.020. Epub 2010 Nov 25.
PMID 21109473
 
The regulation of miRNA-211 expression and its role in melanoma cell invasiveness.
Mazar J, DeYoung K, Khaitan D, Meister E, Almodovar A, Goydos J, Ray A, Perera RJ.
PLoS One. 2010 Nov 1;5(11):e13779. doi: 10.1371/journal.pone.0013779.
PMID 21072171
 
Identification of microRNAs inhibiting TGF-beta-induced IL-11 production in bone metastatic breast cancer cells.
Pollari S, Leivonen SK, Perala M, Fey V, Kakonen SM, Kallioniemi O.
PLoS One. 2012;7(5):e37361. doi: 10.1371/journal.pone.0037361. Epub 2012 May 21.
PMID 22629385
 
MicroRNA-204/211 alters epithelial physiology.
Wang FE, Zhang C, Maminishkis A, Dong L, Zhi C, Li R, Zhao J, Majerciak V, Gaur AB, Chen S, Miller SS.
FASEB J. 2010 May;24(5):1552-71. doi: 10.1096/fj.08-125856. Epub 2010 Jan 7.
PMID 20056717
 
Differential expression of microRNAs during melanoma progression: miR-200c, miR-205 and miR-211 are downregulated in melanoma and act as tumour suppressors.
Xu Y, Brenn T, Brown ER, Doherty V, Melton DW.
Br J Cancer. 2012 Jan 31;106(3):553-61. doi: 10.1038/bjc.2011.568. Epub 2012 Jan 5.
PMID 22223089
 

Citation

This paper should be referenced as such :
Avan, A ; Maftouh, M ; Peters, GJ ; Giovannetti, E
MIR211 (microRNA 211)
Atlas Genet Cytogenet Oncol Haematol. 2013;17(11):753-756.
Free journal version : [ pdf ]   [ DOI ]
On line version : http://AtlasGeneticsOncology.org/Genes/MIR211ID50533ch15q13.html


External links

Nomenclature
HGNC (Hugo)MIR211   31588
Cards
AtlasMIR211ID50533ch15q13
Entrez_Gene (NCBI)MIR211  406993  microRNA 211
AliasesMIRN211; mir-211
GeneCards (Weizmann)MIR211
Ensembl hg19 (Hinxton)ENSG00000207702 [Gene_View]
Ensembl hg38 (Hinxton)ENSG00000207702 [Gene_View]  chr15:31065032-31065141 [Contig_View]  MIR211 [Vega]
ICGC DataPortalENSG00000207702
TCGA cBioPortalMIR211
AceView (NCBI)MIR211
Genatlas (Paris)MIR211
WikiGenes406993
SOURCE (Princeton)MIR211
Genetics Home Reference (NIH)MIR211
miRBaseMIR211
dbDEMCMIR211
Genomic and cartography
GoldenPath hg38 (UCSC)MIR211  -     chr15:31065032-31065141 -  15q13.3   [Description]    (hg38-Dec_2013)
GoldenPath hg19 (UCSC)MIR211  -     15q13.3   [Description]    (hg19-Feb_2009)
EnsemblMIR211 - 15q13.3 [CytoView hg19]  MIR211 - 15q13.3 [CytoView hg38]
Mapping of homologs : NCBIMIR211 [Mapview hg19]  MIR211 [Mapview hg38]
OMIM613753   
Gene and transcription
Genbank (Entrez)AJ550414 LM608356
RefSeq transcript (Entrez)
RefSeq genomic (Entrez)NC_000015 NC_018926 NG_016453 NT_187660 NW_011332701
Consensus coding sequences : CCDS (NCBI)MIR211
Alternative Splicing GalleryENSG00000207702
Gene ExpressionMIR211 [ NCBI-GEO ]   MIR211 [ EBI - ARRAY_EXPRESS ]   MIR211 [ SEEK ]   MIR211 [ MEM ]
Gene Expression Viewer (FireBrowse)MIR211 [ Firebrowse - Broad ]
SOURCE (Princeton)Expression in : [Datasets]   [Normal Tissue Atlas]  [carcinoma Classsification]  [NCI60]
BioGPS (Tissue expression)406993
GTEX Portal (Tissue expression)MIR211
Human Protein AtlasENSG00000207702-MIR211 [pathology]   [cell]   [tissue]
Protein : pattern, domain, 3D structure
Domain families : Pfam (Sanger)
Domain families : Pfam (NCBI)
Conserved Domain (NCBI)MIR211
DMDM Disease mutations406993
Blocks (Seattle)MIR211
Human Protein Atlas [tissue]ENSG00000207702-MIR211 [tissue]
Protein Interaction databases
FunCoupENSG00000207702
BioGRIDMIR211
STRING (EMBL)MIR211
ZODIACMIR211
Ontologies - Pathways
Huge Navigator MIR211 [HugePedia]
snp3D : Map Gene to Disease406993
BioCentury BCIQMIR211
ClinGenMIR211
Clinical trials, drugs, therapy
Chemical/Protein Interactions : CTD406993
Chemical/Pharm GKB GenePA164722592
Clinical trialMIR211
Miscellaneous
canSAR (ICR)MIR211 (select the gene name)
Probes
Litterature
PubMed29 Pubmed reference(s) in Entrez
GeneRIFsGene References Into Functions (Entrez)
CoreMineMIR211
EVEXMIR211
GoPubMedMIR211
iHOPMIR211
REVIEW articlesautomatic search in PubMed
Last year publicationsautomatic search in PubMed

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indexed on : Wed Nov 15 12:27:24 CET 2017

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