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MIR26A1 (microRNA 26a-1)

Written2011-11Bo Zhang, Qian Zhao
Institute of Biochemistry, Cell Biology, Chinese Academy of Sciences, Shanghai, 200031, China (BZ); Department of Pathophysiology, Shanghai Jiao-Tong University, School of Medicine, Shanghai, 200030, China (QZ)

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Identity

Other aliasMIR26A
MIRN26A1
LocusID (NCBI) 407015
Atlas_Id 51208
Location 3p22.2  [Link to chromosome band 3p22]
Location_base_pair Starts at and ends at bp from pter
Local_order Within one intron of CTDSPL (CTD (carboxy-terminal domain, RNA polymerase II, polypeptide A) small phosphatase-like, CTDSPL).
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

Note The 22-bp precursor microRNA 26a-1 holds complete conservation among Human, Rhesus, Mouse and Dog. MIR26A1 functions as tumor suppressor gene in hepatocellular carcinoma (Ji et al., 2009; Kota et al., 2009), breast cancer (Zhang et al., 2011), rhabdomyosarcoma (Ciarapica et al., 2009) and MYC-induced lymphoma (Sander et al., 2008). Additionally, MIR26A1 potentially plays an important role in regulating IFN-β anti-inflammatory signaling (Witwer et al., 2010).
 
  The precursor MIR26A1 is composed of 77 nucleotides and its stem-loop structure is shown here. The sequence of mature MIR26A1 is marked in red.
Description The precursor MIR26A1 maps on chromosome 3p22.2 spanning 77 bp and is located within one intron of CTDSPL (CTD (carboxy-terminal domain, RNA polymerase II, polypeptide A) small phosphatase-like, CTDSPL).
Transcription The MIR26A1 gene is initially transcribed as a primary transcript in the nucleus and then further processed by the Drosha-Pasha/DGCR8 complex as an intermediate named the precursor microRNA 26a-1. After exported into cytoplasm by Exportin-5, the precursor microRNA 26a-1 was cleaved by Dicer as a duplex and in turn forms the mature 22-bp MIR26A1.

Mutations

Note None.

Implicated in

Note
  
Entity Hepatocellular carcinoma (HCC)
Note MIR26A is reduced in hepatocellular carcinoma and directly suppresses the expression of ERα (estrogen receptor alpha, ERα) (Chen et al., 2011), cyclin D2 and cyclin E2 (Kota et al., 2009). The overexpression of MIR26A negatively regulates cell proliferation (Chen et al., 2011) and cell cycle (Kota et al., 2009). Systemic administration of MIR26A in a mouse model of HCC using adeno-associated virus (AAV) results in inhibition of cancer cell proliferation, induction of tumor-specific apoptosis, and dramatic protection from disease progression without toxicity (Kota et al., 2009).
  
  
Entity Nasopharyngeal carcinoma (NPC)
Note MIR26A is commonly downregulated in NPC specimens and NPC cell lines and directly suppresses the expression of EZH2 (enhancer of zeste homolog 2, EZH2) (Lu et al., 2011). Ectopic expression of MIR26A inhibits growth and colony formation of NPC cells by inducing G1-phase cell-cycle arrest. MIR26A also suppresses tumorigenesis of NPC cells in vivo. MIR26A suppressed the expression of c-myc, cyclins D3 and E2, and cyclin-dependent kinases CDK4 and CDK6 while enhancing the expression of CDK inhibitors p14ARF and p21CIP1 in an EZH2-dependent manner.
  
  
Entity Breast cancer
Note MIR26A is downregulated in breast cancer specimens and cell lines and directly regulates the expression of MTDH (metadherin, MTDH) and EZH2 (Zhang et al., 2011). MIR26A leads to apoptosis, inhibition of colony forming and in vivo tumorigenesis of breast cancer cells.
  
  
Entity Rhabdomyosarcoma
Note In rhabdomyosarcoma, MIR26A is underexpressed while the mRNA of EZH2 is increased. EZH2 is one of direct targets of MIR26A in several different cell lines (Ciarapica et al., 2009; Lu et al., 2011; Zhang et al., 2011).
  
  
Entity Airway smooth muscle hypertrophy
Note Stretch selectively induces the transcription of MIR26A in human airway smooth muscle cells (HASMCs). The transcription factor CCAAT enhancer-binding protein α (C/EBPα) directly activates miR-26a expression through the transcriptional machinery upon stretch. Glycogen synthase kinase-3β (GSK-3β) is a direct target of MIR26A (Mohamed et al., 2010). The enforced expression of MIR26A induces HASMC hypertrophy.
  
  
Entity Myogenesis
Note MIR26A is up-regulated during myogenesis and directly targets EZH2. Overexpression of MIR26A in murine myogenic C2C12 cells induced creatine kinase activity. Moreover, myoD and myogenin mRNA expression levels were also up-regulated. Therefore, increased expression of miR-26a promotes myogenesis (Wong and Tellam, 2008).
  
  
Entity Osteogenic differentiation
Note During hADSC (human adipose tissue-derived stem cells, hADSCs) differentiation, MIR26A shows increased expression. The inhibition of miR-26a increases protein levels of its predicted target, SMAD1 transcription factor (Luzi et al., 2008).
  

Bibliography

Tumor-specific expression of microRNA-26a suppresses human hepatocellular carcinoma growth via cyclin-dependent and -independent pathways.
Chen L, Zheng J, Zhang Y, Yang L, Wang J, Ni J, Cui D, Yu C, Cai Z.
Mol Ther. 2011 Aug;19(8):1521-8. doi: 10.1038/mt.2011.64. Epub 2011 May 24.
PMID 21610700
 
Deregulated expression of miR-26a and Ezh2 in rhabdomyosarcoma.
Ciarapica R, Russo G, Verginelli F, Raimondi L, Donfrancesco A, Rota R, Giordano A.
Cell Cycle. 2009 Jan 1;8(1):172-5. Epub 2009 Jan 30.
PMID 19106613
 
MicroRNA expression, survival, and response to interferon in liver cancer.
Ji J, Shi J, Budhu A, Yu Z, Forgues M, Roessler S, Ambs S, Chen Y, Meltzer PS, Croce CM, Qin LX, Man K, Lo CM, Lee J, Ng IO, Fan J, Tang ZY, Sun HC, Wang XW.
N Engl J Med. 2009 Oct 8;361(15):1437-47.
PMID 19812400
 
Therapeutic microRNA delivery suppresses tumorigenesis in a murine liver cancer model.
Kota J, Chivukula RR, O'Donnell KA, Wentzel EA, Montgomery CL, Hwang HW, Chang TC, Vivekanandan P, Torbenson M, Clark KR, Mendell JR, Mendell JT.
Cell. 2009 Jun 12;137(6):1005-17.
PMID 19524505
 
MiR-26a inhibits cell growth and tumorigenesis of nasopharyngeal carcinoma through repression of EZH2.
Lu J, He ML, Wang L, Chen Y, Liu X, Dong Q, Chen YC, Peng Y, Yao KT, Kung HF, Li XP.
Cancer Res. 2011 Jan 1;71(1):225-33.
PMID 21199804
 
Osteogenic differentiation of human adipose tissue-derived stem cells is modulated by the miR-26a targeting of the SMAD1 transcription factor.
Luzi E, Marini F, Sala SC, Tognarini I, Galli G, Brandi ML.
J Bone Miner Res. 2008 Feb;23(2):287-95.
PMID 18197755
 
Mechanical stretch up-regulates microRNA-26a and induces human airway smooth muscle hypertrophy by suppressing glycogen synthase kinase-3b.
Mohamed JS, Lopez MA, Boriek AM.
J Biol Chem. 2010 Sep 17;285(38):29336-47. Epub 2010 Jun 3.
PMID 20525681
 
MYC stimulates EZH2 expression by repression of its negative regulator miR-26a.
Sander S, Bullinger L, Klapproth K, Fiedler K, Kestler HA, Barth TF, Moller P, Stilgenbauer S, Pollack JR, Wirth T.
Blood. 2008 Nov 15;112(10):4202-12. Epub 2008 Aug 19.
PMID 18713946
 
MicroRNA regulation of IFN-beta protein expression: rapid and sensitive modulation of the innate immune response.
Witwer KW, Sisk JM, Gama L, Clements JE.
J Immunol. 2010 Mar 1;184(5):2369-76. Epub 2010 Feb 3.
PMID 20130213
 
MicroRNA-26a targets the histone methyltransferase Enhancer of Zeste homolog 2 during myogenesis.
Wong CF, Tellam RL.
J Biol Chem. 2008 Apr 11;283(15):9836-43. Epub 2008 Feb 15.
PMID 18281287
 
Pathologically decreased miR-26a antagonizes apoptosis and facilitates carcinogenesis by targeting MTDH and EZH2 in breast cancer.
Zhang B, Liu XX, He JR, Zhou CX, Guo M, He M, Li MF, Chen GQ, Zhao Q.
Carcinogenesis. 2011 Jan;32(1):2-9. Epub 2010 Oct 15.
PMID 20952513
 

Citation

This paper should be referenced as such :
Zhang, B ; Zhao, Q
MIR26A1 (microRNA 26a-1)
Atlas Genet Cytogenet Oncol Haematol. 2012;16(4):278-279.
Free journal version : [ pdf ]   [ DOI ]
On line version : http://AtlasGeneticsOncology.org/Genes/MIR26A1ID51208ch3p22.html


External links

Nomenclature
Cards
AtlasMIR26A1ID51208ch3p22.txt
Aliases
Genomic and cartography
Gene and transcription
RefSeq transcript (Entrez)
RefSeq genomic (Entrez)
SOURCE (Princeton)Expression in : [Datasets]   [Normal Tissue Atlas]  [carcinoma Classsification]  [NCI60]
BioGPS (Tissue expression)407015
Protein : pattern, domain, 3D structure
Domain families : Pfam (Sanger)
Domain families : Pfam (NCBI)
Protein Interaction databases
Ontologies - Pathways
Clinical trials, drugs, therapy
Miscellaneous
canSAR (ICR) (select the gene name)
Probes
Litterature
REVIEW articlesautomatic search in PubMed
Last year publicationsautomatic search in PubMed


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