mir-1 microRNA precursor family

mir-1 microRNA precursor family
mIR-1 microRNA precursor family
Symbol mir-1
Rfam RF00103
miRBase MI0000651
miRBase family MIPF0000038
Entrez 406904
OMIM 609326
Other data
RNA type Gene; miRNA;
Domain(s) Metazoa
GO 0035195
SO 0001244
Locus Chr. 20 q13.33

The miR-1 microRNA precursor is a small micro RNA that regulates its target protein's expression in the cell. microRNAs are transcribed as ~70 nucleotide precursors and subsequently processed by the Dicer enzyme to give a ~22 nucleotide products. In this case the mature sequence comes from the 3' arm of the precursor. The mature products are thought to have regulatory roles through complementarity to mRNA. In humans there are two distinct microRNAs that share an identical mature sequence, these are called miR-1-1 and miR-1-2.

These micro RNAs have pivotal roles in development and physiology of muscle tissues including the heart[1][2]. MiR-1 is known to be involved in important role in heart diseases such as hypertrophy, myocardial infarction, and arrhythmias [3][4][5]. Studies have shown that MiR-1 is an important regulator of heart adaption after ischemia or ischaemic stress and it is upregulated in the remote myocardium of patients with myocardial infarction[6]. Also MiR-1 is downregulated in myocardial infarcted tissue compared to healthy heart tissue [7]. Plasma levels of MiR-1 can be used as a sensitive biomarker for myocardial infarction [8].


Targets of miR-1

The heat shock protein, HSP60 is also known to be a target for post-transcriptional regulation by miR-1 and miR-206. HSP60 is a component of the defence mechanism against diabetic myocardial injury and its level is reduced in the diabetic myocardium. In both in vivo and in vitro experiments increased levels of glucose in myocardiomyctes led to significant upregulation of miR-1 and miR-206 with resulting modulation of HSP60 leading to accelerated glucose-mediated apoptosis in cardiomyocetes.[9] The level of HSP70 is also a target for post-transcriptional repression by MiR-1.[10]

MiR-1 has key roles in the development and differentiation of smooth and skeletal muscles [11][12][13]. For example in the lineage-specific differention of smooth muscle cells from embroyonic stem cell derived cultures, MiR-1 is required; as its loss of function resulted in a reduction in smooth muscle cell biomarkers and a reduction in the derived smooth muscle cell population. There is evidence that the control of smooth muscle cell differentiation by MiR-1 may be mediated by the down regulation of Kruppel-like factor 4 (KLF4), since a MiR-1 recognition site is predicted in the 3' UTR of KLF4 and inhibition of MiR-1 results in reversed down-regulation of KLF4 and an inhibition of smooth muscle cell differentiation[14]. A mutation in the 3' UTR of the myostatin gene in Texel sheep creates a miR-1 and miR-206 target site. This is likely to cause the muscular phenotype of this breed of sheep.[15]

Clinical relevance of miR-1

Mir-1 plays an important role in some cancers. Rhabdomyosarcoma is the most common soft tissue sarcoma in children. Since the tumor results from undifferentiated cells, agents that promote differentiation hold promise as possible therapies. A study showed that levels of mir-1 and mir-133a were drastically reduced in tumourous cell lines whilst their targets were up-regulated [16].

Introduction of miR-1 and miR-133a into an embryonal rhabdomyosarcoma-derived cell line is cytostatic, which suggested a strong tumour-suppressive role for these microRNAs. Expression of miR-1 but not miR-133a gave transcriptional profiles that were consistent with a strong promyogenic influence on the cells, again demonstrating the role of miR-1 in muscle differentiation from precursor stem cells. The authors propose that miR-1 and miR-133a act to repress isoforms of genes that are not normally expressed in muscle cells. All of these observations suggest that mis-regulation of miR-1 and miR-133a can result in tumorogeneis via abolition of the supressive effect they have on certain gene targets and of the removal of the promotion of differentiation of the cells exerted my miR-1 [16].

The involvement of miR-1 in cancer is not limited to cancers of muscle and muscle tissues. MiR-1 may have a tumour-suppressive effect in bladder cancer by regulation of LIM and SH3 protein 1 (LASP1) [17]. In lung cancer there is evidence for the down-regulation of miR-1 [18].

There is evidence for the role of miR-1-2 as a modulator in acute myeloid leukemia via its transcription by the zinc-finger transcription factor, EVI1, ectopic virus expression site 1. ChIP assays have shown that EVI1 binds strongly to the promoters of miR-1-2 and miR-133-a-1, and expression of EVI1 is significantly correlated with the expression of miR-1-2 and miR-133-a-1 in established cell lines and in patient samples. However, only miR-1-2 was involved in abnormal proliferation in EVI1 expressing cell lines [19].


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Further reading

  1. ^ Chen J, Yin H, Jiang Y, Radhakrishnan SK, Huang ZP, Li J, Shi Z, Catharina EP, Gui Y, Wang DZ, Zheng XL (2010). "Induction of MicroRNA-1 by Myocardin in Smooth Muscle Cells Inhibits Cell Proliferation.". Arterioscler Thromb Vasc Biol 31 (2): 368–375. doi:10.1161/ATVBAHA.110.218149. PMID 21051663. 
  2. ^ Sumiyoshi K, Kubota S, Ohgawara T, Kawata K, Nishida T, Shimo T, Yamashiro T, Takigawa M (2010). "Identification of miR-1 as a micro RNA that supports late-stage differentiation of growth cartilage cells.". Biochem Biophys Res Commun 402 (2): 286–90. doi:10.1016/j.bbrc.2010.10.016. PMID 20937250. 
  3. ^ Xie C, Huang H, Sun X, Guo Y, Hamblin M, Ritchie RP, Garcia-Barrio MT, Zhang J, Chen YE (2010). "MicroRNA-1 Regulates Smooth Muscle Cell Differentiation by Repressing Kruppel-Like Factor 4.". Stem Cells Dev 20 (2): 205–210. doi:10.1089/scd.2010.0283. PMID 20799856. 
  4. ^ Li Q, Song XW, Zou J, Wang GK, Kremneva E, Li XQ, Zhu N, Sun T, Lappalainen P, Yuan WJ, Qin YW, Jing Q (2010). "Attenuation of microRNA-1 derepresses the cytoskeleton regulatory protein twinfilin-1 to provoke cardiac hypertrophy.". J Cell Sci 123 (Pt 14): 2444–52. doi:10.1242/jcs.067165. PMID 20571053. 
  5. ^ Jiang Y, Yin H, Zheng XL (2010). "MicroRNA-1 inhibits myocardin-induced contractility of human vascular smooth muscle cells.". J Cell Physiol 225 (2): 506–11. doi:10.1002/jcp.22230. PMID 20458751. 
  6. ^ Cheng Y, Tan N, Yang J, Liu X, Cao X, He P, Dong X, Qin S, Zhang C (2010). "A translational study of circulating cell-free microRNA-1 in acute myocardial infarction.". Clin Sci (Lond) 119 (2): 87–95. doi:10.1042/CS20090645. PMID 20218970. 
  7. ^ Sluijter JP, van Mil A, van Vliet P, Metz CH, Liu J, Doevendans PA, Goumans MJ (2010). "MicroRNA-1 and -499 regulate differentiation and proliferation in human-derived cardiomyocyte progenitor cells.". Arterioscler Thromb Vasc Biol 30 (4): 859–68. doi:10.1161/ATVBAHA.109.197434. PMID 20081117. 
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