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MIR22 (microRNA 22)

Written2012-04Juanjuan Zhu, Yongge Wu, Xiaofei Zheng
Jiling university,Changchun 130012, PR China (JZ, YW); Beijing Institute of Radiation Medicine, Beijing 100850, PR China (JZ, XZ)

(Note : for Links provided by Atlas : click)

Identity

Alias_namesMIRN22
Alias_symbol (synonym)hsa-mir-22
Other aliasmiR-22
HGNC (Hugo) MIR22
LocusID (NCBI) 407004
Atlas_Id 51495
Location 17p13.3  [Link to chromosome band 17p13]
Location_base_pair Starts at 1713903 and ends at 1713987 bp from pter ( according to hg19-Feb_2009)  [Mapping MIR22.png]
Local_order Based on Mapviewer (Master Map: Genes on sequence), genes flanking miR-22 oriented from centromere to telomere on 17p13.3 are:
- PRPF8 (17p13.3): PRP8 pre-mRNA processing factor 8 homolog
- TLCD2 (17p13.3): TLC domain containing 2
- MIR22HG (17p13.3): MIR22 host gene
- MIR22 (17p13.3): microRNA22
- WDR81 (17p13.3): WD repeat domain 81
- SERPINF2 (17p13.3): serpin peptidase inhibitor, clade F member 2.

DNA/RNA

 
  Figure1. A. Stem-loop structure of miR-22. B. Genomic localization of miR-22 (MIRN22), miR-22HG (MIRN22HG) on chromosomal band 17p13.3.
Description Mir-22 was originally identified in HeLa cells (an immortal cell line derived from cervical cancer cells), but was later found to be ubiquitously expressed in various tissues. The gene encoding miR-22 is found on the short arm of chromosome 17, in a minimal loss of heterozygosity region.
Transcription In general,the microRNA genes are transcribed by RNA polymerase II, whereas RNA polymerase III is also responsible for transcription of some other microRNAs.
Pre-microRNA 22 (Precursor microRNA)
- Accession: MI0000078.
- Length: 85 bp.
- Sequence:
5'-GGCUGAGCCGCAGUAGUUCUUCAGUGGCAAGCUUUAUGUCCUGACCC
AGCUAAAGCUGCCAGUUGAAGAACUGUUGCCCUCUGCC- 3'
Mature miR-22
Accession: MIMAT0000077.
Length: 22 nucleotides.
Sequence: 53 -AAGCUGCCAGUUGAAGAACUGU- 74
Pseudogene No pseudogenes were reported for mir-22.

Protein

Note MicroRNAs are not translated into amino acids.

Implicated in

Note
  
Entity Breast carcinoma
Note Recently, researchers have found that microRNAs (miRNAs) may play important roles in cancer development. After verification in many clinical samples, among all the miRNAs, there is a significantly inverse association between the miR-22 level and ERα protein expression. Estrogen receptors (ERs) are composed of a group of ligand-activated nuclear receptors that regulate diverse gene expression and are implicated in cancers by stimulating cell proliferation and tumor growth. All experimental data demonstrate that ERα is a direct target of miR-22. Taken together, it indicates that miR-22 is frequently downregulated in ERα-positive human breast cancer cell lines and clinical samples. Because ERα expression level is routinely detected in breast cancer samples as a prognostic marker, that miR-22 is directly involved in the regulation of ERα may be one of the mechanisms through which miR-22 could play a pivotal role in the pathogenesis of breast cancer. The expression of the tumor suppressor miR-22 is consistently downregulated in metastatic breast cancer cells. Oncogenes ERBB3, CDC25C and EVI-1 are abundant in metastatic breast cells. Introduction of miR-22 reduces the level of ERBB3 and EVI-1 as well as phosphor-AKT, an EVI-1 downstream target. It suggests that metastatic cancer cells increase specific oncogenic signaling factors through downregulating of miRNA.
  
  
Entity Ovarian cancer
Note miR-22 level is decreased in ovarian cancer cells which have high invasiveness. Both gain-of-function and loss-of-function study display a negative effect of miR-22 on cell invasion and migration in vitro. Bioinformatics analyses show that miR-22 may regulate multiple pro-metastatic genes. Particularly, Tiam1 is a direct target of miR-22. Alteration of miR-22 expression level has a negative regulatory effect on Tiam1 protein level and mRNA level. Taken together, all findings suggest that miR-22 might be involved in inhibiting ovarian cancer metastasis, probably by targeting Tiam1.
  
  
Entity Hepatocellular carcinoma
Note In present study, a functional role of miR-22 in hepatocellular carcinoma (HCC) development has been identified. It exists in a large proportion of HCC tissues that miR-22 level is downregulated. Epigenetic alternations in cancer often mediate the deregulation of tumor suppressors or oncogenes, and HDAC4 expression targeted by miR-22 may further aggravate the epigenetic changes in HCC. In vivo and in vitro, the anti-tumor effect of miR-22 in HCC is validated. Restoration of miR-22 expression suppresses cell proliferation and tumourigenicity. In addition to HDAC4, miR-22 can also repress Max expression and cell cycle progression regulated by Myc-Max complex. Thus, accumulation of all targets of miR-22 constitutes the phenotype of miR-22 restoration in HCC. Furthermore, miR-22 may have considerable potential in identification of HCC and therapy for HCC.
  
  
Entity Tumor suppressor
Note Oncogenic c-Myc can modulate the expression of a subset of miRNAs, including miR-22, conversely, miR-22 represses the c-Myc-binding protein MYCBP, a positive regulator of c-Myc. MYCBP is a direct target of miR-22. Moreover, repression of MYCBP by miR-22 downregulates a subset of E-box-containing c-Myc target genes.
  
  
Entity Cellular senescence
Note Generally, it is believed that microRNA is associated with cell proliferation, cell differentiation and other biological phenomena. MicroRNA will increase when the aged normal cells stop dividing. Aging extent of cancer cell is suppressed when miR22 is added into cultured breast and cervical cancer cells. It is also found that metastasis of breast cancer is controlled in mouse experiments. Cell aging is a self-defense mechanism which prevents development of cancer in organism. Cell aging will be interfered when microRNA decreases, thus, it promoting cancer cytogenesis. However, aging process in organism restores after addition of miR22, and then proliferation of cancer cell is inhibited.
  

Bibliography

MicroRNA-22 is induced by vitamin D and contributes to its antiproliferative, antimigratory and gene regulatory effects in colon cancer cells.
Alvarez-Diaz S, Valle N, Ferrer-Mayorga G, Lombardia L, Herrera M, Dominguez O, Segura MF, Bonilla F, Hernando E, Munoz A.
Hum Mol Genet. 2012 May 15;21(10):2157-65. Epub 2012 Feb 10.
PMID 22328083
 
miR-22 promotes HBV-related hepatocellular carcinoma development in males.
Jiang R, Deng L, Zhao L, Li X, Zhang F, Xia Y, Gao Y, Wang X, Sun B.
Clin Cancer Res. 2011 Sep 1;17(17):5593-603. Epub 2011 Jul 12.
PMID 21750200
 
Role of epigenetic and miR-22 and miR-29b alterations in the downregulation of Mat1a and Mthfr genes in early preneoplastic livers in rats induced by 2-acetylaminofluorene.
Koturbash I, Melnyk S, James SJ, Beland FA, Pogribny IP.
Mol Carcinog. 2011 Dec 27. doi: 10.1002/mc.21861. [Epub ahead of print]
PMID 22213190
 
Human microRNAs miR-22, miR-138-2, miR-148a, and miR-488 are associated with panic disorder and regulate several anxiety candidate genes and related pathways.
Muinos-Gimeno M, Espinosa-Parrilla Y, Guidi M, Kagerbauer B, Sipila T, Maron E, Pettai K, Kananen L, Navines R, Martin-Santos R, Gratacos M, Metspalu A, Hovatta I, Estivill X.
Biol Psychiatry. 2011 Mar 15;69(6):526-33. Epub 2010 Dec 17.
PMID 21168126
 
Circulating microRNAs involved in multiple sclerosis.
Siegel SR, Mackenzie J, Chaplin G, Jablonski NG, Griffiths L.
Mol Biol Rep. 2012 May;39(5):6219-25. Epub 2012 Jan 10.
PMID 22231906
 
Profiling of immune-related microRNA expression in human cord blood and adult peripheral blood cells upon proinflammatory stimulation.
Takahashi N, Nakaoka T, Yamashita N.
Eur J Haematol. 2012 Jan;88(1):31-8. doi: 10.1111/j.1600-0609.2011.01707.x. Epub 2011 Nov 17.
PMID 21913990
 
MicroRNA-22 promotes cell survival upon UV radiation by repressing PTEN.
Tan G, Shi Y, Wu ZH.
Biochem Biophys Res Commun. 2012 Jan 6;417(1):546-51. Epub 2011 Dec 7.
PMID 22166214
 
Tumor suppressor miR-22 determines p53-dependent cellular fate through post-transcriptional regulation of p21.
Tsuchiya N, Izumiya M, Ogata-Kawata H, Okamoto K, Fujiwara Y, Nakai M, Okabe A, Schetter AJ, Bowman ED, Midorikawa Y, Sugiyama Y, Aburatani H, Harris CC, Nakagama H.
Cancer Res. 2011 Jul 1;71(13):4628-39. Epub 2011 May 12.
PMID 21565979
 
Tumor-suppressive microRNA-22 inhibits the transcription of E-box-containing c-Myc target genes by silencing c-Myc binding protein.
Xiong J, Du Q, Liang Z.
Oncogene. 2010 Sep 2;29(35):4980-8. Epub 2010 Jun 21.
PMID 20562918
 
An estrogen receptor alpha suppressor, microRNA-22, is downregulated in estrogen receptor alpha-positive human breast cancer cell lines and clinical samples.
Xiong J, Yu D, Wei N, Fu H, Cai T, Huang Y, Wu C, Zheng X, Du Q, Lin D, Liang Z.
FEBS J. 2010 Apr;277(7):1684-94. Epub 2010 Feb 17.
PMID 20180843
 
Emerging roles of microRNA-22 in human disease and normal physiology.
Xiong J.
Curr Mol Med. 2012 Mar;12(3):247-58. (REVIEW)
PMID 22300138
 
Attenuation of microRNA-22 derepressed PTEN to effectively protect rat cardiomyocytes from hypertrophy.
Xu XD, Song XW, Li Q, Wang GK, Jing Q, Qin YW.
J Cell Physiol. 2012 Apr;227(4):1391-8. doi: 10.1002/jcp.22852.
PMID 21618527
 
MicroRNA-22 regulates hypoxia signaling in colon cancer cells.
Yamakuchi M, Yagi S, Ito T, Lowenstein CJ.
PLoS One. 2011;6(5):e20291. Epub 2011 May 23.
PMID 21629773
 
microRNA-22, downregulated in hepatocellular carcinoma and correlated with prognosis, suppresses cell proliferation and tumourigenicity.
Zhang J, Yang Y, Yang T, Liu Y, Li A, Fu S, Wu M, Pan Z, Zhou W.
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PMID 20842113
 
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Overexpression of members of the microRNA-183 family is a risk factor for lung cancer: a case control study.
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PMID 21920043
 

Citation

This paper should be referenced as such :
Zhu, J ; Wu, Y ; Zheng, X
MIR22 (microRNA 22)
Atlas Genet Cytogenet Oncol Haematol. 2012;16(10):700-702.
Free journal version : [ pdf ]   [ DOI ]
On line version : http://AtlasGeneticsOncology.org/Genes/MIR22ID51495ch17p13.html


External links

Nomenclature
HGNC (Hugo)MIR22   31599
Cards
AtlasMIR22ID51495ch17p13
Entrez_Gene (NCBI)MIR22  407004  microRNA 22
AliasesMIRN22; hsa-mir-22; miR-22
GeneCards (Weizmann)MIR22
Ensembl hg19 (Hinxton) [Gene_View]
Ensembl hg38 (Hinxton) [Gene_View]  chr17:1713903-1713987 [Contig_View]  MIR22 [Vega]
TCGA cBioPortalMIR22
AceView (NCBI)MIR22
Genatlas (Paris)MIR22
WikiGenes407004
SOURCE (Princeton)MIR22
Genetics Home Reference (NIH)MIR22
miRBaseMIR22
dbDEMCMIR22
Genomic and cartography
GoldenPath hg38 (UCSC)MIR22  -     chr17:1713903-1713987 -  17p13.3   [Description]    (hg38-Dec_2013)
GoldenPath hg19 (UCSC)MIR22  -     17p13.3   [Description]    (hg19-Feb_2009)
EnsemblMIR22 - 17p13.3 [CytoView hg19]  MIR22 - 17p13.3 [CytoView hg38]
Mapping of homologs : NCBIMIR22 [Mapview hg19]  MIR22 [Mapview hg38]
OMIM612077   
Gene and transcription
Genbank (Entrez)AF480525 AJ421742 LM608167
RefSeq transcript (Entrez)
RefSeq genomic (Entrez)NC_000017 NC_018928 NG_032811 NT_187611
Consensus coding sequences : CCDS (NCBI)MIR22
Gene ExpressionMIR22 [ NCBI-GEO ]   MIR22 [ EBI - ARRAY_EXPRESS ]   MIR22 [ SEEK ]   MIR22 [ MEM ]
Gene Expression Viewer (FireBrowse)MIR22 [ Firebrowse - Broad ]
SOURCE (Princeton)Expression in : [Datasets]   [Normal Tissue Atlas]  [carcinoma Classsification]  [NCI60]
BioGPS (Tissue expression)407004
GTEX Portal (Tissue expression)MIR22
Protein : pattern, domain, 3D structure
Domain families : Pfam (Sanger)
Domain families : Pfam (NCBI)
Conserved Domain (NCBI)MIR22
DMDM Disease mutations407004
Blocks (Seattle)MIR22
Protein Interaction databases
BioGRIDMIR22
STRING (EMBL)MIR22
ZODIACMIR22
Ontologies - Pathways
Huge Navigator MIR22 [HugePedia]
snp3D : Map Gene to Disease407004
BioCentury BCIQMIR22
ClinGenMIR22
Clinical trials, drugs, therapy
Chemical/Protein Interactions : CTD407004
Chemical/Pharm GKB GenePA164722605
Clinical trialMIR22
Miscellaneous
canSAR (ICR)MIR22 (select the gene name)
Probes
Litterature
PubMed94 Pubmed reference(s) in Entrez
GeneRIFsGene References Into Functions (Entrez)
CoreMineMIR22
EVEXMIR22
GoPubMedMIR22
iHOPMIR22
REVIEW articlesautomatic search in PubMed
Last year publicationsautomatic search in PubMed

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indexed on : Fri Jun 30 11:11:51 CEST 2017

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