View source for MiR-214

{{Infobox rfam
| Name = miR-214
| image =Mir-214 SS.png
| width =
| caption = Conserved [[secondary structure]] of miR-214 microRNA precursor
| Symbol = miR-214
| AltSymbols = MIR214
| Rfam = RF00660
| miRBase = MI0000290
| miRBase_family = MIPF0000062
| RNA_type = miRNA
| Tax_domain = [[Metazoa]]
| GO = 0035195
| SO = 0001244
| CAS_number =
| EntrezGene = 406996
| HGNCid = 31591
| OMIM = 610721
| PDB =
| RefSeq = NR_029627
| Chromosome = 1
| Arm = q
| Band = 24.3
| LocusSupplementaryData =
}} {{lowercase}} __NOTOC__
'''miR-214''' is a vertebrate-specific family of [[microRNA]] precursors. The ~22&nbsp;[[nucleotide]] mature miRNA sequence is excised from the precursor hairpin by the enzyme [[Dicer]].<ref>{{cite journal | vauthors = Ambros V | title = microRNAs: tiny regulators with great potential | journal = Cell | volume = 107 | issue = 7 | pages = 823–6 | date = December 2001 | pmid = 11779458 | doi = 10.1016/S0092-8674(01)00616-X | s2cid = 14574186 | doi-access = free }}</ref> This sequence then associates with [[RNA-induced silencing complex|RISC]] which effects [[RNA interference]].<ref>{{cite journal | vauthors = Gregory RI, Chendrimada TP, Cooch N, Shiekhattar R | title = Human RISC couples microRNA biogenesis and posttranscriptional gene silencing | journal = Cell | volume = 123 | issue = 4 | pages = 631–40 | date = November 2005 | pmid = 16271387 | doi = 10.1016/j.cell.2005.10.022 | s2cid = 16973870 | doi-access = free }}</ref>
==Origin and evolution of miR-214==
miR-214 is a vertebrate-specific miR family that possesses one member in non-teleost vertebrates and two members in teleost fish. miR-214 is likely to have emerged within the [[DNM3|Dnm3]] gene after the divergence of [[Jawed vertebrate|jawed]] and [[jawless vertebrates]] and is located on the opposite strand of an intron of Dnm3 and is associated in an expression cluster with [[Mir-199 microRNA precursor|miR-199]].<ref name="Desvignes & Postlethwait 2013">{{cite journal | vauthors = Desvignes T, Contreras A, Postlethwait JH | title = Evolution of the miR199-214 cluster and vertebrate skeletal development | journal = RNA Biology | volume = 11 | issue = 4 | pages = 281–94 | year = 2014 | pmid = 24643020 | pmc = 4075512 | doi = 10.4161/rna.28141 }}</ref>
== Function ==
miR-214 is a "melano-miR",<ref name="Bar11">{{cite journal | vauthors = Bar-Eli M | title = Searching for the 'melano-miRs': miR-214 drives melanoma metastasis | journal = The EMBO Journal | volume = 30 | issue = 10 | pages = 1880–1 | date = May 2011 | pmid = 21593728 | pmc = 3098491 | doi = 10.1038/emboj.2011.132 }}</ref> so-called because it is thought to encourage the [[metastasis]] of [[melanoma]]. Specifically, the mature microRNA excised from miR-214 is predicted to target two [[activating protein 2]] transcription factors, bringing about downstream effects on a number of genes regulating vital [[cell cycle]] processes, such as [[apoptosis]], [[cell growth|proliferation]] and [[angiogenesis]].<ref name="Bar11" />
miR-214 is also thought to regulate [[type-I collagen]].<ref>{{cite journal | vauthors = Maubach G, Lim MC, Chen J, Yang H, Zhuo L | title = miRNA studies in in vitro and in vivo activated hepatic stellate cells | journal = World Journal of Gastroenterology | volume = 17 | issue = 22 | pages = 2748–73 | date = June 2011 | pmid = 21734783 | pmc = 3122263 | doi = 10.3748/WJG.v17.i22.2748 | doi-access = free }}</ref>
==Role in cancer==
miR-214 has been found to be downregulated in human [[cervical cancer]]; when miR-214 was upregulated in [[HeLa]] cancer cells, it was found to significantly reduce cell growth.<ref name="Yan09">{{cite journal | vauthors = Yang Z, Chen S, Luan X, Li Y, Liu M, Li X, Liu T, Tang H | title = MicroRNA-214 is aberrantly expressed in cervical cancers and inhibits the growth of HeLa cells | journal = IUBMB Life | volume = 61 | issue = 11 | pages = 1075–82 | date = November 2009 | pmid = 19859982 | doi = 10.1002/iub.252 | s2cid = 19360060 | doi-access = free }}</ref> Two [[mRNA]] targets were identified as those encoding the proteins [[MAP2K3]] and [[MAPK8]].<ref name="Yan09" />
The increased expression of miR-214 in [[pancreatic cancer]] could bring about increased resistance to [[chemotherapy]].<ref>{{cite journal | vauthors = Zhang XJ, Ye H, Zeng CW, He B, Zhang H, Chen YQ | title = Dysregulation of miR-15a and miR-214 in human pancreatic cancer | journal = Journal of Hematology & Oncology | volume = 3 | pages = 46 | date = November 2010 | pmid = 21106054 | pmc = 3002909 | doi = 10.1186/1756-8722-3-46 | doi-access = free }}</ref>
In human [[glioma]] cell line T98G expression of miR-214 has been shown to suppress expression of the [[ubiquitin]]-conjugating enzyme 9 (UBC9) and reduces [[tumour]] cell proliferation.  The protein UBC9 is involved in the [[SUMO protein|sumoylation pathway]], and is up-regulated in many cancers.<ref name="pmid23187003">{{cite journal | vauthors = Zhao Z, Tan X, Zhao A, Zhu L, Yin B, Yuan J, Qiang B, Peng X | title = microRNA-214-mediated UBC9 expression in glioma | journal = BMB Reports | volume = 45 | issue = 11 | pages = 641–6 | date = November 2012 | pmid = 23187003 | doi = 10.5483/BMBRep.2012.45.11.097 | url = http://www.bmbreports.org/fulltext/bmbreports/view.php?vol=45&page=641 | archive-url = https://web.archive.org/web/20160303224655/http://www.bmbreports.org/fulltext/bmbreports/view.php?vol=45&page=641 | url-status = dead | archive-date = 2016-03-03 | pmc = 4133799 }}</ref>
==Implication of miR-214 in skeletogenesis==
miR-214, along with its cluster mate [[Mir-199 microRNA precursor|miR-199]], has been shown to be implicated in skeleton formation. miR-214 has been shown to inhibit bone formation in human cell lines both by targeting [[ATF4]],<ref>{{cite journal | vauthors = Wang X, Guo B, Li Q, Peng J, Yang Z, Wang A, Li D, Hou Z, Lv K, Kan G, Cao H, Wu H, Song J, Pan X, Sun Q, Ling S, Li Y, Zhu M, Zhang P, Peng S, Xie X, Tang T, Hong A, Bian Z, Bai Y, Lu A, Li Y, He F, Zhang G, Li Y | title = miR-214 targets ATF4 to inhibit bone formation | journal = Nature Medicine | volume = 19 | issue = 1 | pages = 93–100 | date = January 2013 | pmid = 23223004 | doi = 10.1038/nm.3026 | s2cid = 16207561 }}</ref> a gene encoding one of the maintranscription factors required for osteoblast function and by suppressing osteogenic differentiation of [[C2C12]] myoblast cells by targeting [[Sp7 transcription factor|Sp7]],<ref>{{cite journal | vauthors = Shi K, Lu J, Zhao Y, Wang L, Li J, Qi B, Li H, Ma C | title = MicroRNA-214 suppresses osteogenic differentiation of C2C12 myoblast cells by targeting Osterix | journal = Bone | volume = 55 | issue = 2 | pages = 487–94 | date = August 2013 | pmid = 23579289 | doi = 10.1016/j.bone.2013.04.002 }}</ref> an osteoblast-specific transcription factor. Also, [[TWIST-1|Twist-1]], which is a major actor in skeleton formation, regulates miR-199 and miR-214 cluster expression in mouse.<ref>{{cite journal | vauthors = Lee YB, Bantounas I, Lee DY, Phylactou L, Caldwell MA, Uney JB | title = Twist-1 regulates the miR-199a/214 cluster during development | journal = Nucleic Acids Research | volume = 37 | issue = 1 | pages = 123–8 | date = January 2009 | pmid = 19029138 | pmc = 2615617 | doi = 10.1093/nar/gkn920 }}</ref> Furthermore, miR199-214 cluster deletion in mouse lead to skeletal development abnormalities including craniofacial defects, neural arch and spinous processes malformations, and osteopenia.<ref>{{cite journal | vauthors = Burkardt DD, Rosenfeld JA, Helgeson ML, Angle B, Banks V, Smith WE, Gripp KW, Moline J, Moran RT, Niyazov DM, Stevens CA, Zackai E, Lebel RR, Ashley DG, Kramer N, Lachman RS, Graham JM | title = Distinctive phenotype in 9 patients with deletion of chromosome 1q24-q25 | journal = American Journal of Medical Genetics. Part A | volume = 155A | issue = 6 | pages = 1336–51 | date = June 2011 | pmid = 21548129 | pmc = 3109510 | doi = 10.1002/ajmg.a.34049 }}</ref> In zebrafish, miR-214 expression is mainly observed around developing skeletal elements.<ref name="Desvignes & Postlethwait 2013" />
== References ==
{{reflist|30em}}
{{miRNA precursor families}}
[[Category:MicroRNA]]