miR-138

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miR-138
File:Mir-138 SS.png
Conserved secondary structure of miR-138 prescursor
Identifiers
SymbolmiR-138
RfamRF00671
miRBaseMI0000476
miRBase familyMIPF0000075
Entrez406929
HUGO31524
Other data
RNA typemiRNA
Domain(s)Animalia
LocusChr. 3 p
PDB structuresPDBe

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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  13. ↑ Murchison EP, Kheradpour P, Sachidanandam R, Smith C, Hodges E, Xuan Z, Kellis M, Grützner F, Stark A, Hannon GJ (Jun 2008). "Conservation of small RNA pathways in platypus". Genome Research. 18 (6): 995–1004. doi:10.1101/gr.073056.107. PMC 2413167. PMID 18463306.
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  18. ↑ Friedländer MR, Chen W, Adamidi C, Maaskola J, Einspanier R, Knespel S, Rajewsky N (Apr 2008). "Discovering microRNAs from deep sequencing data using miRDeep". Nature Biotechnology. 26 (4): 407–15. doi:10.1038/nbt1394. PMID 18392026.
  19. ↑ Hackl M, Jakobi T, Blom J, Doppmeier D, Brinkrolf K, Szczepanowski R, Bernhart SH, Höner Zu Siederdissen C, Bort JA, Wieser M, Kunert R, Jeffs S, Hofacker IL, Goesmann A, Pühler A, Borth N, Grillari J (Apr 2011). "Next-generation sequencing of the Chinese hamster ovary microRNA transcriptome: Identification, annotation and profiling of microRNAs as targets for cellular engineering". Journal of Biotechnology. 153 (1–2): 62–75. doi:10.1016/j.jbiotec.2011.02.011. PMC 3119918. PMID 21392545.
  20. ↑ Chen PY, Manninga H, Slanchev K, Chien M, Russo JJ, Ju J, Sheridan R, John B, Marks DS, Gaidatzis D, Sander C, Zavolan M, Tuschl T (Jun 2005). "The developmental miRNA profiles of zebrafish as determined by small RNA cloning". Genes & Development. 19 (11): 1288–93. doi:10.1101/gad.1310605. PMC 1142552. PMID 15937218.
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  29. ↑ Zhou M, Wang Q, Sun J, Li X, Xu L, Yang H, Shi H, Ning S, Chen L, Li Y, He T, Zheng Y (Aug 2009). "In silico detection and characteristics of novel microRNA genes in the Equus caballus genome using an integrated ab initio and comparative genomic approach". Genomics. 94 (2): 125–31. doi:10.1016/j.ygeno.2009.04.006. PMID 19406225.
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  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. PMC 2783372. PMID 19540661.
  35. ↑ 35.0 35.1 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. PMC 3544506. 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. 127 (3): 505–12. doi:10.1002/ijc.25320. PMC 2885137. PMID 20232393.

Further reading

External links

Category:MicroRNA

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