miR-138

miR-138
Conserved secondary structure of miR-138 prescursor
Identifiers
Symbol miR-138
Rfam RF00671
miRBase MI0000476
miRBase family MIPF0000075
Entrez 406929
HUGO 31524
Other data
RNA type miRNA
Domain(s) Animalia
Locus Chr. 3 p

miR-138 is a family of microRNA precursors found in animals, including humans.[1] MicroRNAs are typically transcribed as ~70 nucleotide precursors and subsequently processed by the Dicer enzyme to give a ~22 nucleotide product.[2] The excised region or, mature product, of the miR-138 precursor is the microRNA mir-138.

miR-138 has been used as an example of the post-transcriptional regulation of miRNA, due to the finding that while the precursor is expressed ubiquitously, the mature product is found only in specific cell types.[3]

Species distribution

The presence of miR-138 has been detected experimentally in humans (Homo sapiens)[1][4][5] and in different animals including house mouse (Mus musculus),[1][3][4][6][7][8][9] brown rat (Rattus norvegicus),[1][7][10][11][12] platypus (Ornithorhynchus anatinus),[13] Carolina anole(Anolis carolinensis),[14] cattle (Bos taurus),[15][16] common carp (Cyprinus carpio),[17] dog (Canis familiaris),[18] Chinese hamster (Cricetulus griseus),[19] zebrafish (Danio rerio),[20] red junglefowl (Gallus gallus),[21] western gorilla (Gorilla gorilla),[22] gray short-tailed opossum (Monodelphis domestica),[23] Oryzias latipes,[24] sea lamprey (Petromyzon marinus),[25] Tasmanian devil (Sarcophilus harrisii),[26] wild boar (Sus scrofa)[27] and zebra finch (Taeniopygia guttata).[28]

It is also predicted computationally that the miR-138 gene exists in the genome of other animals including horse (Equus caballus),[29] rhesus macaque (Macaca mulatta),[30] takifugu rubripes (Fugu rubripes), Bornean orangutan (Pongo pygmaeus),[31] common chimpanzee (Pan troglodytes),[32] Tetraodon nigroviridis and western clawed frog (Xenopus tropicalis).

Genomic location

In human genome, there are two miR-138 associated genes and they are not located in any cluster. More precisely, the miR-138-1 gene is in region 5 at 3p21.3[33] and miR-138-2 is located on chromosome 16 (16q13).[34]

Pattern of expression

In adult mice, miR-138 is only expressed in brain tissue. Its expression is not uniform throughout the brain but restricted to distinct neuronal populations. On the contrary, its precursor, pre-miR-138-2, is ubiquitously expressed throughout all tissues, which suggests that the expression of miRNAs can be regulated at the post-transcription level.[3]

In the zebrafish, miR-138 is expressed in specific domains in the heart and is required to establish appropriate chamber-specific gene expression patterns.[35]

Targets and function

Since the identification of miR-138, a number of targets have been found and some of them have been verified experimentally. It has been proven that miR-138 is involved in different pathways. Furthermore, it is in relation with various types of cancer.

HIF-1a
Hypoxia-inducible factor-1alpha (HIF-1a), one of the key regulators in cancer cells, has been shown to be one target of miR-138.[36]
VIM, ZEB2, EZH2 and head and neck cancers
Downregulation of miR-138 has been reported in several types of cancers, including HNSCC(head and neck squamous cell carcinoma). It is suggested that miR-138 is a multi-functional molecular regulator and plays major roles in EMT (epithelial-mesenchymal transition) and in HNSCC progression. A number of miR-138 target genes have been identified to be associated with EMT, including VIM (vimentin), ZEB2 (zinc finger E-box-binding homeobox 2) and EZH2 (enhancer of zeste homologue 2).[37]
CCND1 and nasopharyngeal carcinoma
miR-138 is commonly underexpressed in nasopharyngeal carcinoma (NPC) specimens and NPC cell lines. Cyclin D1 (CCND1), which is widely upregulated in NPC tumors, is found as a direct target of miR-138. Therefore, miR-138 might be a tumor suppressor in NPC, which is exerted partially by inhibiting CCND1 expression.[38]
BCR-ABL and CCND3
BCR (breakpoint cluster region)-ABL (c-abl oncogene 1, non-receptor tyrosine kinase)/GATA1/miR-138 mini circuitry contributes to the leukemogenesis of chronic myeloid leukemia (CML). ABL and BCR-ABL are the target genes of miR-138, which binds to the coding region instead of three prime untranslated region (3'UTR). miR-138 can negatively regulate another gene CCND3 via binding to its 3'-UTR. The expression of miR-138 is activated by GATA1, which in turn is repressed by BCR-ABL. Therefore, miR-138, by virtue of a BCR-ABL/GATA1/miR-138 circuitry, is a tumor suppressor miRNA implicated in the pathogenesis of CML and its clinical response to imatinib.[39]
H2AX and DNA damage repair
mir-138 is linked with DNA damage repair. It can directly target the histone H2AX 3'UTR, reduce histone H2AX expression and induce chromosomal instability after DNA damage.[40]
ALDH1A2 and CSPG2
In zebrafish, the mature form of miR-138 regulates gene expression influencing cardiac development. miR-138 helps establish discrete domains of gene expression during cardiac morphogenesis by targeting multiple members of a common pathway. It has been experimentally verified that miR-138 can negatively regulate aldh1a2, encoding retinoic acid (RA) dehydrogenase (Raldh2), by targeting the binding site in the 3'UTR of its mRNA. Another putative target of miR-138 is cspg2.[35]
Regulation of sleep
In rats, miR-138, let-7b, and miR-125a are expressed at different times and in different structures in the brain and likely play a role in the regulation of sleep.[41]
Brain cancer
miR-138 has been found to be significantly linked with the formation and growth of Gliomas, from Cancerous Stem Cells (CSC). In vitro inhibition of miR-138 prevents tumour sphere formation. Furthermore, its high expression in Glioma makes it a potential biomarker for CSC.[42]
Rhoc, ROCK2 and Tongue cancer
Tumour metastasis concerning the Tongue Squamous Cell Carcinoma (TSCC) can be regulated via the expression of 2 key genes in Rho GTPase signaling pathway : RhoC and ROCK2 (Rho-associated protein kinase 2). Thus, by targeting the 3' untranslated region of those genes, mir-138 is able to reduce their expression and by this mean, to destroy TSCC ability migrate and invade.[43]

References

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  33. ↑ Calin GA, Sevignani C, Dumitru CD, Hyslop T, Noch E, Yendamuri S, Shimizu M, Rattan S, Bullrich F, Negrini M, Croce CM (Mar 2004). "Human microRNA genes are frequently located at fragile sites and genomic regions involved in cancers". Proceedings of the National Academy of Sciences of the United States of America 101 (9): 2999–3004. doi:10.1073/pnas.0307323101. PMC 365734. PMID 14973191.
  34. ↑ Liu X, Jiang L, Wang A, Yu J, Shi F, Zhou X (Dec 2009). "MicroRNA-138 suppresses invasion and promotes apoptosis in head and neck squamous cell carcinoma cell lines". Cancer Letters 286 (2): 217–22. doi:10.1016/j.canlet.2009.05.030. PMID 19540661.
  35. 1 2 Morton SU, Scherz PJ, Cordes KR, Ivey KN, Stainier DY, Srivastava D (Nov 2008). "microRNA-138 modulates cardiac patterning during embryonic development". Proceedings of the National Academy of Sciences of the United States of America 105 (46): 17830–5. doi:10.1073/pnas.0804673105. PMC 2582580. PMID 19004786.
  36. ↑ Song T, Zhang X, Wang C, Wu Y, Cai W, Gao J, Hong B (2011). "MiR-138 suppresses expression of hypoxia-inducible factor 1α (HIF-1α) in clear cell renal cell carcinoma 786-O cells". Asian Pacific Journal of Cancer Prevention 12 (5): 1307–11. PMID 21875287.
  37. ↑ Liu X, Wang C, Chen Z, Jin Y, Wang Y, Kolokythas A, Dai Y, Zhou X (Nov 2011). "MicroRNA-138 suppresses epithelial-mesenchymal transition in squamous cell carcinoma cell lines". The Biochemical Journal 440 (1): 23–31. doi:10.1042/BJ20111006. PMC 3331719. PMID 21770894.
  38. ↑ Liu X, Lv XB, Wang XP, Sang Y, Xu S, Hu K, Wu M, Liang Y, Liu P, Tang J, Lu WH, Feng QS, Chen LZ, Qian CN, Bei JX, Kang T, Zeng YX (Jul 2012). "MiR-138 suppressed nasopharyngeal carcinoma growth and tumorigenesis by targeting the CCND1 oncogene". Cell Cycle 11 (13): 2495–506. doi:10.4161/cc.20898. PMID 22739938.
  39. ↑ Xu C, Fu H, Gao L, Wang L, Wang W, Li J, Li Y, Dou L, Gao X, Luo X, Jing Y, Chim CS, Zheng X, Yu L (Jan 2014). "BCR-ABL/GATA1/miR-138 mini circuitry contributes to the leukemogenesis of chronic myeloid leukemia". Oncogene 33 (1): 44–54. doi:10.1038/onc.2012.557. PMID 23208504.
  40. ↑ Wang Y, Huang JW, Li M, Cavenee WK, Mitchell PS, Zhou X, Tewari M, Furnari FB, Taniguchi T (Aug 2011). "MicroRNA-138 modulates DNA damage response by repressing histone H2AX expression". Molecular Cancer Research 9 (8): 1100–11. doi:10.1158/1541-7786.MCR-11-0007. PMC 3157593. PMID 21693595.
  41. ↑ Davis CJ, Clinton JM, Krueger JM (Dec 2012). "MicroRNA 138, let-7b, and 125a inhibitors differentially alter sleep and EEG delta-wave activity in rats". Journal of Applied Physiology 113 (11): 1756–62. doi:10.1152/japplphysiol.00940.2012. PMID 23104698.
  42. ↑ Chan XH, Nama S, Gopal F, Rizk P, Ramasamy S, Sundaram G, Ow GS, Ivshina AV, Tanavde V, Haybaeck J, Kuznetsov V, Sampath P (Sep 2012). "Targeting glioma stem cells by functional inhibition of a prosurvival oncomiR-138 in malignant gliomas". Cell Reports 2 (3): 591–602. doi:10.1016/j.celrep.2012.07.012. PMID 22921398.
  43. ↑ Jiang L, Liu X, Kolokythas A, Yu J, Wang A, Heidbreder CE, Shi F, Zhou X (Aug 2010). "Downregulation of the Rho GTPase signaling pathway is involved in the microRNA-138-mediated inhibition of cell migration and invasion in tongue squamous cell carcinoma". International Journal of Cancer. Journal International Du Cancer 127 (3): 505–12. doi:10.1002/ijc.25320. PMID 20232393.

Further reading

  • Pignot G, Cizeron-Clairac G, Vacher S, Susini A, Tozlu S, Vieillefond A, Zerbib M, Lidereau R, Debre B, Amsellem-Ouazana D, Bieche I (Jun 2013). "microRNA expression profile in a large series of bladder tumors: identification of a 3-miRNA signature associated with aggressiveness of muscle-invasive bladder cancer". International Journal of Cancer. Journal International Du Cancer 132 (11): 2479–91. doi:10.1002/ijc.27949. PMID 23169479. 
  • Ye D, Wang G, Liu Y, Huang W, Wu M, Zhu S, Jia W, Deng AM, Liu H, Kang J (Aug 2012). "MiR-138 promotes induced pluripotent stem cell generation through the regulation of the p53 signaling". Stem Cells 30 (8): 1645–54. doi:10.1002/stem.1149. PMID 22696098. 
  • Jin Y, Wang C, Liu X, Mu W, Chen Z, Yu D, Wang A, Dai Y, Zhou X (Nov 2011). "Molecular characterization of the microRNA-138-Fos-like antigen 1 (FOSL1) regulatory module in squamous cell carcinoma". The Journal of Biological Chemistry 286 (46): 40104–9. doi:10.1074/jbc.c111.296707. PMID 21969367. 
  • Eskildsen T, Taipaleenmäki H, Stenvang J, Abdallah BM, Ditzel N, Nossent AY, Bak M, Kauppinen S, Kassem M (Apr 2011). "MicroRNA-138 regulates osteogenic differentiation of human stromal (mesenchymal) stem cells in vivo". Proceedings of the National Academy of Sciences of the United States of America 108 (15): 6139–44. doi:10.1073/pnas.1016758108. PMID 21444814. 
  • Muiños-Gimeno M, Espinosa-Parrilla Y, Guidi M, Kagerbauer B, Sipilä T, Maron E, Pettai K, Kananen L, Navinés R, Martín-Santos R, Gratacòs M, Metspalu A, Hovatta I, Estivill X (Mar 2011). "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". Biological Psychiatry 69 (6): 526–33. doi:10.1016/j.biopsych.2010.10.010. PMID 21168126. 
  • Kisliouk T, Yosefi S, Meiri N (Jan 2011). "MiR-138 inhibits EZH2 methyltransferase expression and methylation of histone H3 at lysine 27, and affects thermotolerance acquisition". The European Journal of Neuroscience 33 (2): 224–35. doi:10.1111/j.1460-9568.2010.07493.x. PMID 21070394. 
  • Yang Z, Bian C, Zhou H, Huang S, Wang S, Liao L, Zhao RC (Feb 2011). "MicroRNA hsa-miR-138 inhibits adipogenic differentiation of human adipose tissue-derived mesenchymal stem cells through adenovirus EID-1". Stem Cells and Development 20 (2): 259–67. doi:10.1089/scd.2010.0072. PMID 20486779. 

External links

miRNA precursor families
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Category:MicroRNA

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