mir-181 microRNA precursor

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mir-181 microRNA precursor
Symbol miR-181
Rfam RF00076
miRBase MI0000269
miRBase family MIPF0000007
Other data
RNA type Gene; miRNA
Domain(s) Eukaryota
GO 0035195 0035068
SO 0001244

In molecular biology miR-181 microRNA precursor is a small non-coding RNA molecule. MicroRNAs (miRNAs) are transcribed as ~70 nucleotide precursors and subsequently processed by the RNase-III type enzyme Dicer to give a ~22 nucleotide mature product. In this case the mature sequence comes from the 5' arm of the precursor. They target and modulate protein expression by inhibiting translation and / or inducing degradation of target messenger RNAs. This new class of genes has recently been shown to play a central role in malignant transformation. miRNA are downregulated in many tumors and thus appear to function as tumor suppressor genes.[1] The mature products miR-181a, miR-181b, miR-181c or miR-181d are thought to have regulatory roles at posttranscriptional level, through complementarity to target mRNAs.[2] miR-181 which has been predicted or experimentally confirmed in a wide number of vertebrate species as rat, zebrafish, and in the pufferfish (see below) (MIPF0000007).


It has been shown that miR-181 is preferentially expressed in the B-lymphoid cells of mouse bone marrow,[3] but also in the retina and brain.[4] In humans, this microRNA is involved in the mechanisms of immunity, and in many different cancers (see below) it was found to be expressed at a particularly low level.[5]

Genome location[edit]

miR-181a1 and miR-181b1 are clustered together and located on the chromosome 1 (37.p5), miR-181a2 and miR-181b2 are clustered together and located on the chromosome 9 (37.p5).[6][7][8] miR-181c and miR-181d are clustered together and located on the chromosome 19 (37.p5).[2][9][10]


miR-181 family are present in vertebrates and nematodes[citation needed] (this list is not exhaustive):

miR-181 roles[edit]

Chronic Lymphocytic Leukemia
miR-181 may have a regulatory role with tumor suppressors genes of the human chromosome 1.[5] It has been shown that the Tcl1 oncogene is a target of miR-181a in an inhibition relation (downregulated) that would result in an action on the tumor cell growth process. miR-181 expression has a reverse correlation with Tcl1 protein expression.[31]

mir-181 a and b are over-expressed and act as bad prognosis maker of aggressive neuroblastoma (Stage 4) as compare to low grade stage (Stage 1;2;3 and 4S) whereas mir-181 c and d isoforms are not. In these conditions, they regulate the tumor suppressor gene CDON.[32]

Myoblast Differentiation
It has been shown that miR-181 targets the homeobox protein Hox-A11 and participates in establishing muscle tissue downregulating it (a repressor of the differentiation process in mammalians and lower organisms).[33]

Breast cancer
miR-181a, miR-181b, miR-181c and miR-181d are activated by the human gene ERBB2, located on the chromosome 17. The expression of miR-181c is relevant to characterize a Breast cancer form, the HER2/neu.[34]
miR-181 is also activated by the small molecule tamoxifen.[35] One selective modulators of estrogen receptor having specific activities of tissue. Tamoxifen acts as an anti-estrogen (inhibitor) in breast tissue, but as an estrogen (stimulating agent) in cholesterol metabolism, bone density, and the proliferation of endometrial cells. miR-181 could acquire a resistance to tamoxifen, the drug is successfully used to treat women with estrogen receptor-positive breast cancer.[35]

Acute Myeloid Leukemia
Downregulation of miR-181 family contributes to aggressive leukemia phenotype through mechanisms related to the activation pathways of innate immunity mediated by toll-like receptors TLR2, TLR4, TLR7 and TLR8 and interleukin-1β IL1B (humans on chromose 2).[1]

miR-181a, miR-181b, and miR-181c, which are down-regulated in glioblastoma.[36] miR-181b is downregulated in glioma samples compared with the normal brain tissue. It is suggested that the downregulation of miR-181 may play a role in the development of cancer. It is shown that transfection of miR-181a and miR-181b triggers growth inhibition, apoptosis and inhibits invasion. In addition, the expression of miR-181a was found to be inversely correlated with tumor grading while miR-181b was uniformly downregulated in gliomas with different grades of malignancy.[37]

It has been shown that downregulated miR-181a and miR-181b were also involved in the oncogenesis of gliomas. miR-181a and miR-181b function as tumor suppressors that cause inhibition of growth, induce apoptosis and inhibit invasion of glioma cells. In addition, the tumor suppressive effect of miR-181b in glioma cells was apparent that the effect of miR-181a. These aberrant results suggest that downregulated miR-181a and miR-181b may be key factors that contribute to the occurrence in malignant human gliomas.[38]

Multiple Myeloma
MiRNA signature for multiple myeloma (MM) has been described, including miR-181a and miR-181b, which modulate the expression of proteins essential for the pathogenesis of myeloma. Xenograft studies using human MM cell lines treated with miR-181a and miR-181b antagonists resulted in significant suppression of tumor growth in nude mice.[39]

Papillary Thyroid Carcinoma
It was found that miR-181a and miR-181c are overexpressed in Papillary Thyroid Carcinoma tumors, sufficiently to successfully predict cancer status.[40]

Hepatocellular carcinoma
It has been shown that conserved miR-181 family were upregulated in EpCAM+ AFP+ Hepatocellular carcinoma (HCC) cells and EpCAM+ HCC isolated from AFP+ tumors. In addition, miR-181 family members were highly expressed in the embryonic liver and isolated hepatic stem cells. Especially, inhibition of miR-181 leads to a reduction of the EpCAM+, the amount of HCC cells and initiate tumor capacity, whereas exogenous miR-181 expression in HCC cells resulted in an enrichment of EpCAM+ HCC cells. miR-181 could directly target hepatic transcriptional regulators of differentiation (like homeobox 2 CDX2 and 6 GATA proteins binding GATA6) and an inhibitor of Wnt / beta-catenin. It suggests that miR-181 may eradicate HCC.[41]

miR-181a roles[edit]

T cell Sensitivity

The increased expression of miR-181a in mature T cells increases susceptibility to peptide antigens, while inhibiting the expression of miR-181a in immature T cells reduces sensitivity and alters the both positive and negative selection. In addition, the quantitative regulation of the sensitivity of T cells by miR-181a allows for mature T cells recognize peptide inhibitor antagonists, like agonists. These effects are achieved in part by downregulation of multiple phosphatases, which leads to high levels of steadystate phosphorylated intermediates and reducing the threshold of T cell receptor signaling. The expression of miR-181a correlates with a greater sensitivity of immature T cells in T cells, suggesting that miR-181a acts as an antigen intrinsic sensitivity "rheostat" during the development of T cells.[42]

Vascular Development
It has been shown that miR-181a binds the 3' UTR of Prox1 leading to translation repression and transcript degradation. Prox1 is a homeobox transcription factor involved in development of the lymphatic endothelium.[43]

Cerebellar Neurodegeneration
miR-181a has a relatively broad expression pattern and is present in neurons in numerous parts of the mouse brain. miR-181a is essential for the survival of Purkinje cells and its absence leads to a slow degeneration of these cells.[44]

Diabetes Mellitus
It has been shown that there are significant correlations between the expression of miR-181a and both adipose tissue morphology and key metabolic parameters, including visceral fat area, HbA1c, fasting plasma glucose, and circulating leptin, adiponectin, interleukin-6. The expression of miR-181a may contribute to intrinsic differences between omental and subcutaneous adipose tissue.[45]

Homozygous Sickle Cell Disease
miR-181a is over-represented in the normal hemoglobin (HbAA) erythrocytes.[46] miR-181a has been shown to play a role in the lineage differentiation in the hematopoietic system.[3]

miR-181b roles[edit]

Colorectal Cancer

miR-181b was significantly overexpressed in tumors compared to normal colorectal samples, especially high miR-181b expression correlated with poor survival of only black patients with stage III colorectal cancers [47] (Sequencing analysis revealed that miR-181b expression is strongly associated with mutation status of the tumor suppressor gene p53.[48]

Cardiac Hypertrophy
miR-181b is downregulated during hypertrophy, it causes a reduction in cardiomyocyte cell size.[49]

Oral Carcinoma
miR-181b expression was steadily increased and is associated with increased severity of lesions during the progression of the Oral Carcinoma. Overexpression of miR-181b may play an important role in malignant transformation.[50]

Prostate Cancer
miR-181b is downregulated in cancerous cells.[51]

Adrenocortical carcinoma

Mir-210 has been suggested as a useful biomarker to distinguish adrenocortical carcinoma from adrenocortical adenoma.[52]

miR-181c roles[edit]

in Apoptosis

miR-181d roles[edit]

Duchenne Muscular Dystrophy miR-181d is disregulated in Duchenne Muscular Dystrophy (DMD).[53]

Nemaline Myopathy
miR-181d is disregulated in Nemaline Myopathy (NM).[53]


  1. ^ a b Larson RA. (2010). "Micro-RNAs and copy number changes: new levels of gene regulation in acute myeloid leukemia.". Chem Biol Interact. 184 (1-2): 21–5. doi:10.1016/j.cbi.2009.10.002. PMC 2846194Freely accessible. PMID 19822134. 
  2. ^ a b c d Lim LP, Glasner ME, Yekta S, Burge CB, Bartel DP, et al. (2003). "Vertebrate microRNA genes". Science. 299 (5612): 1540. doi:10.1126/science.1080372. PMID 12624257. 
  3. ^ a b Chen CZ, Li L, Lodish HF, Bartel DP (2004). "MicroRNAs modulate hematopoietic lineage differentiation". Science. 303 (5654): 83–6. doi:10.1126/science.1091903. PMID 14657504. 
  4. ^ Ryan DG, Oliveira-Fernandes M, Lavker RM (2006). "MicroRNAs of the mammalian eye display distinct and overlapping tissue specificity". Mol. Vis. 12: 1175–84. PMID 17102797. 
  5. ^ a b S Marton; MR Garcia; C Robello; H Persson; F Trajtenberg; O Pritsch; C Rovira; H Naya; G Dighiero; A Cayota (2008). "Small RNAs analysis in CLL reveals a deregulation of miRNA expression and novel miRNA candidates of putative relevance in CLL pathogenesis". Leukemia. 22 (2): 330–338. doi:10.1038/sj.leu.2405022. PMID 17989717. 
  6. ^ Lui WO, Pourmand N, Patterson BK, Fire A (2007). "Patterns of known and novel small RNAs in human cervical cancer". Cancer Res. 67 (13): 6031–43. doi:10.1158/0008-5472.CAN-06-0561. PMID 17616659. 
  7. ^ Cai X, Lu S, Zhang Z, Gonzalez CM, Damania B, Cullen BR (2005). "Kaposi's sarcoma-associated herpesvirus expresses an array of viral microRNAs in latently infected cells". Proc Natl Acad Sci U S A. 102 (15): 5570–5. doi:10.1073/pnas.0408192102. PMC 556237Freely accessible. PMID 15800047. 
  8. ^ Dostie J, Mourelatos Z, Yang M, Sharma A, Dreyfuss G (2003). "Numerous microRNPs in neuronal cells containing novel microRNAs". RNA. 9 (2): 180–6. doi:10.1261/rna.2141503. PMC 1370383Freely accessible. PMID 12554860. 
  9. ^ Landgraf P, Rusu M, Sheridan R, Sewer A, Iovino N, Aravin A, Pfeffer S, Rice A, Kamphorst AO, Landthaler M, Lin C, Socci ND, Hermida L, Fulci V, Chiaretti S, Foa R, Schliwka J, Fuchs U, Novosel A, Muller RU, Schermer B, Bissels U, Inman J, Phan Q, Chien M (2007). "A mammalian microRNA expression atlas based on small RNA library sequencing". Cell. 129 (7): 1401–1414. doi:10.1016/j.cell.2007.04.040. PMC 2681231Freely accessible. PMID 17604727. 
  10. ^ Bentwich I, Avniel A, Karov Y, Aharonov R, Gilad S, Barad O, Barzilai A, Einat P, Einav U, Meiri E, Sharon E, Spector Y, Bentwich Z (2005). "Identification of hundreds of conserved and nonconserved human microRNAs". Nat. Genet. 37 (7): 766–70. doi:10.1038/ng1590. PMID 15965474. 
  11. ^ Lyson TR, Sperling EA, Heimberg AM, Gauthier JA, King BL, Peterson KJ (2012). "MicroRNAs support a turtle + lizard clade". Biol Lett. 8 (1): 104–7. doi:10.1098/rsbl.2011.0477. PMC 3259949Freely accessible. PMID 21775315. 
  12. ^ Strozzi F, Mazza R, Malinverni R, Williams JL (2009). "Annotation of 390 bovine miRNA genes by sequence similarity with other species". Anim. Genet. 40 (1): 125. doi:10.1111/j.1365-2052.2008.01780.x. PMID 18945293. 
  13. ^ Jin W, Grant JR, Stothard P, Moore SS, Guan LL (2009). "Characterization of bovine miRNAs by sequencing and bioinformatics analysis". BMC Mol Biol. 10: 90. doi:10.1186/1471-2199-10-90. PMC 2761914Freely accessible. PMID 19758457.  open access publication – free to read
  14. ^ Yan X, Ding L, Li Y, Zhang X, Liang Y, Sun X, Teng CB (2012). "Identification and profiling of microRNAs from skeletal muscle of the common carp". PLOS ONE. 7 (1): e30925. doi:10.1371/journal.pone.0030925. PMC 3267759Freely accessible. PMID 22303472.  open access publication – free to read
  15. ^ Friedlander MR, Chen W, Adamidi C, Maaskola J, Einspanier R, Knespel S, Rajewsky N (2008). "Discovering microRNAs from deep sequencing data using miRDeep". Nat. Biotechnol. 26 (4): 407–15. doi:10.1038/nbt1394. PMID 18392026. 
  16. ^ Hackl M, Jakobi T, Blom J, Doppmeier D, Brinkrolf K, Szczepanowski R, Bernhart SH, Siederdissen CH, Bort JA, Wieser M, Kunert R, Jeffs S, Hofacker IL, Goesmann A, Puhler A, Borth N, Grillari J (2011). "Next-generation sequencing of the Chinese hamster ovary microRNA transcriptome: Identification, annotation and profiling of microRNAs as targets for cellular engineering". J Biotechnol. 153 (1-2): 62–75. doi:10.1016/j.jbiotec.2011.02.011. PMC 3119918Freely accessible. PMID 21392545. 
  17. ^ Zhou M, Wang Q, Sun J, Li X, Xu L, Yang H, Shi H, Ning S, Chen L, Li Y, He T, Zheng Y (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. 
  18. ^ International Chicken Genome Sequencing Consortium (2004). "Sequence and comparative analysis of the chicken genome provide unique perspectives on vertebrate evolution". Nature. 432 (7018): 695–716. doi:10.1038/nature03154. PMID 15592404. 
  19. ^ Yao Y, Zhao Y, Xu H, Smith LP, Lawrie CH, Watson M, Nair V (2008). "MicroRNA profile of Marek's disease virus-transformed T-cell line MSB-1: predominance of virus-encoded microRNAs". J Virol. 82 (8): 4007–15. doi:10.1128/JVI.02659-07. PMC 2293013Freely accessible. PMID 18256158. 
  20. ^ a b c d e f g h Berezikov E, Guryev V, van de Belt J, Wienholds E, Plasterk RH, Cuppen E (2005). "Phylogenetic shadowing and computational identification of human microRNA genes". Cell. 120 (1): 21–4. doi:10.1016/j.cell.2004.12.031. PMID 15652478. 
  21. ^ Devor EJ, Samollow PB (2008). "In vitro and in silico annotation of conserved and nonconserved microRNAs in the genome of the marsupial Monodelphis domestica". J Hered. 99 (1): 66–72. doi:10.1093/jhered/esm085. PMID 17965199. 
  22. ^ Weber MJ (2005). "New human and mouse microRNA genes found by homology search". FEBS J. 272 (1): 59–73. doi:10.1111/j.1432-1033.2004.04389.x. PMID 15634332. 
  23. ^ Murchison EP, Kheradpour P, Sachidanandam R, Smith C, Hodges E, Xuan Z, Kellis M, Grutzner F, Stark A, Hannon GJ (2008). "Conservation of small RNA pathways in platypus". Genome Res. 18 (6): 995–1004. doi:10.1101/gr.073056.107. PMC 2413167Freely accessible. PMID 18463306. 
  24. ^ Li SC, Chan WC, Ho MR, Tsai KW, Hu LY, Lai CH, Hsu CN, Hwang PP, Lin WC (2010). "Discovery and characterization of medaka miRNA genes by next generation sequencing platform". BMC Genomics. 11 Suppl 4: S8. doi:10.1186/1471-2164-11-S4-S8. PMC 3005926Freely accessible. PMID 21143817.  open access publication – free to read
  25. ^ Heimberg AM, Cowper-Sal-lari R, Semon M, Donoghue PC, Peterson KJ (2010). "microRNAs reveal the interrelationships of hagfish, lampreys, and gnathostomes and the nature of the ancestral vertebrate". Proc Natl Acad Sci USA. 107 (45): 19379–83. doi:10.1073/pnas.1010350107. PMC 2984222Freely accessible. PMID 20959416. 
  26. ^ Linsen SE, de Wit E, de Bruijn E, Cuppen E (2010). "Small RNA expression and strain specificity in the rat". BMC Genomics. 11: 249. doi:10.1186/1471-2164-11-249. PMC 2864251Freely accessible. PMID 20403161.  open access publication – free to read
  27. ^ Murchison EP, Tovar C, Hsu A, Bender HS, Kheradpour P, Rebbeck CA, Obendorf D, Conlan C, Bahlo M, Blizzard CA, Pyecroft S, Kreiss A, Kellis M, Stark A, Harkins TT, Marshall Graves JA, Woods GM, Hannon GJ, Papenfuss AT (2010). "The Tasmanian devil transcriptome reveals Schwann cell origins of a clonally transmissible cancer". Science. 327 (5961): 84–7. doi:10.1126/science.1180616. PMC 2982769Freely accessible. PMID 20044575. 
  28. ^ Reddy AM, Zheng Y, Jagadeeswaran G, Macmil SL, Graham WB, Roe BA, Desilva U, Zhang W, Sunkar R (2009). "Cloning, characterization and expression analysis of porcine microRNAs". BMC Genomics. 10: 65. doi:10.1186/1471-2164-10-65. PMC 2644714Freely accessible. PMID 19196471.  open access publication – free to read
  29. ^ Warren WC, Clayton DF, Ellegren H, Arnold AP, Hillier LW, Kunstner A, Searle S, White S, Vilella AJ, Fairley S, Heger A, Kong L, Ponting CP, Jarvis ED, Mello CV, Minx P, Lovell P, Velho TA, Ferris M, Balakrishnan CN, Sinha S, Blatti C, London SE, Li Y, Li (2010). "The genome of a songbird". Nature. 464 (7289): 757–62. doi:10.1038/nature08819. PMC 3187626Freely accessible. PMID 20360741. 
  30. ^ Tang GQ, Maxwell ES (2008). "Xenopus microRNA genes are predominantly located within introns and are differentially expressed in adult frog tissues via post-transcriptional regulation". Genome Res. 18 (1): 104–12. doi:10.1101/gr.6539108. PMC 2134782Freely accessible. PMID 18032731. 
  31. ^ Pekarsky Y, Santanam U, Cimmino A, et al. (2006). "Tcl1 expression in chronic lymphocytic leukemia is regulated by miR-29 and miR-181". Cancer Res. 66 (24): 11590–3. doi:10.1158/0008-5472.CAN-06-3613. PMID 17178851. 
  32. ^ Gibert b (Nov 2014). "Regulation by miR181 Family of the Dependence Receptor CDON Tumor Suppressive Activity in Neuroblastoma.". J Natl Cancer Inst. 106 (11): dju318. doi:10.1093/jnci/dju318. PMID 25313246. 
  33. ^ Naguibneva I, Ameyar-Zazoua M, Polesskaya A, et al. (2006). "The microRNA miR-181a targets the homeobox protein Hox-A11 during mammalian myoblast differentiation". Nat. Cell Biol. 8 (3): 278–84. doi:10.1038/ncb1373. PMID 16489342. 
  34. ^ Lowery AJ, Miller N, Devaney A, McNeill RE, Davoren PA, Lemetre C, Benes V, Schmidt S, Blake J, Ball G, Kerin MJ (2009). "MicroRNA signatures predict oestrogen receptor, progesterone receptor and HER2/neu receptor status in breast cancer". Breast Cancer Res. 11 (3): R27. doi:10.1186/bcr2257. PMC 2716495Freely accessible. PMID 19432961. 
  35. ^ a b Miller TE, Ghoshal K, Ramaswamy B, Roy S, Datta J, Shapiro CL, Jacob S, Majumder S (2008). "MicroRNA-221/222 confers tamoxifen resistance in breast cancer by targeting p27Kip1". J Biol Chem. 283 (44): 29897–29903. doi:10.1074/jbc.M804612200. PMC 2573063Freely accessible. PMID 18708351. 
  36. ^ Ciafre SA, Galardi S, Mangiola A, Ferracin M, Liu CG, Sabatino G, Negrini M, Maira G, Croce CM, Farace MG (2005). "Extensive modulation of a set of microRNAs in primary glioblastoma.". Biochem Biophys Res Commun. 334 (4): 1351–8. doi:10.1016/j.bbrc.2005.07.030. PMID 16039986. 
  37. ^ Conti A, Aguennouz M, La Torre D, Tomasello C, Cardali S, Angileri FF, Maio F, Cama A, Germanò A, Vita G, Tomasello F (2009). "miR-21 and 221 upregulation and miR-181b downregulation in human grade II-IV astrocytic tumors.". Journal of Neuro-Oncology. 93 (3): 325–32. doi:10.1007/s11060-009-9797-4. PMID 19159078. 
  38. ^ Shi L, Cheng Z, Zhang J, Li R, Zhao P, Fu Z, You Y (2008). "hsa-mir-181a and hsa-mir-181b function as tumor suppressors in human glioma cells.". Brain Res. 1236: 185–93. doi:10.1016/j.brainres.2008.07.085. PMID 18710654. 
  39. ^ Pichiorri F, Suh SS, Ladetto M, Kuehl M, Palumbo T, Drandi D, Taccioli C, Zanesi N, Alder H, Hagan JP (2008). "MicroRNAs regulate critical genes associated with multiple myeloma pathogenesis.". Proc Natl Acad Sci USA. 105 (35): 12885–90. doi:10.1073/pnas.0806202105. PMC 2529070Freely accessible. PMID 18728182. 
  40. ^ He H, Jazdzewski K, Li W, Liyanarachchi S, Nagy R, Volinia S, Calin GA, Liu CG, Franssila K, Suster S, Kloos RT, Croce CM, de la Chapelle A (2005). "The role of microRNA genes in papillary thyroid carcinoma.". Proc Natl Acad Sci USA. 102 (52): 19075–80. doi:10.1073/pnas.0509603102. PMC 1323209Freely accessible. PMID 16365291. 
  41. ^ Ji J, Yamashita T, Budhu A, Forgues M, Jia HL, Li C (2009). "Identification of microRNA-181 by genome-wide screening as a critical player in EpCAM-positive hepatic cancer stem cells.". Hepatology. 50 (2): 472–80. doi:10.1002/hep.22989. PMC 2721019Freely accessible. PMID 19585654. 
  42. ^ Qi-Jing Li; Jacqueline Chau; Peter J.R. Ebert; Giselle Sylvester; Hyeyoung Min; Gwen Liu; Ravi Braich; Muthiah Manoharan; Juergen Soutschek; Petra Skare; Lawrence O. Klein; Mark M. Davis & Chang-Zheng Chen (2007). "miR-181a Is an Intrinsic Modulator of T Cell Sensitivity and Selection". Cell. 129 (1): 147–161. doi:10.1016/j.cell.2007.03.008. PMID 17382377. 
  43. ^ Kazenwadel J, Michael MZ, Harvey NL (June 2010). "Prox1 expression is negatively regulated by miR-181 in endothelial cells". Blood. 116 (13): 2395–2401. doi:10.1182/blood-2009-12-256297. PMID 20558617. 
  44. ^ Schaefer A, O'Carroll D, Tan CL, Hillman D, Sugimori M, Llinas R, Greengard P (2007). "Cerebellar neurodegeneration in the absence of microRNAs.". J Exp Med. 204 (7): 1553–8. doi:10.1084/jem.20070823. PMC 2118654Freely accessible. PMID 17606634. 
  45. ^ Klöting N, Berthold S, Kovacs P, Schön MR, Fasshauer M, Ruschke K, Stumvoll M, Blüher M (2009). "MicroRNA expression in human omental and subcutaneous adipose tissue.". PLOS ONE. 4 (3): e4699. doi:10.1371/journal.pone.0004699. PMC 2649537Freely accessible. PMID 19259271.  open access publication – free to read
  46. ^ Chen SY, Wang Y, Telen MJ, Chi JT (2008). "The genomic analysis of erythrocyte microRNA expression in sickle cell diseases.". PLOS ONE. 3 (6): e2360. doi:10.1371/journal.pone.0002360. PMC 2408759Freely accessible. PMID 18523662.  open access publication – free to read
  47. ^ Bovell LC, Shanmugam C, Putcha BD, Katkoori VR, Zhang B, Bae S, Singh KP, Grizzle WE, Manne U (2013). "The prognostic value of microRNAs varies with patient race/ethnicity and stage of colorectal cancer.". Clin. Cancer Res. 19 (14): 3955–3965. doi:10.1158/1078-0432.CCR-12-3302. PMC 3746330Freely accessible. PMID 23719259. 
  48. ^ Xi Y, Formentini A, Chien M, Weir DB, Russo JJ, Ju J, Kornmann M, Ju J (2006). "Prognostic Values of microRNAs in Colorectal Cancer.". Biomark Insights. 2: 113–121. PMC 2134920Freely accessible. PMID 18079988. 
  49. ^ van Rooij E, Sutherland LB, Liu N, Williams AH, McAnally J, Gerard RD, Richardson JA, Olson EN (2006). "A signature pattern of stress-responsive microRNAs that can evoke cardiac hypertrophy and heart failure.". Proc Natl Acad Sci USA. 103 (48): 18255–60. doi:10.1073/pnas.0608791103. PMC 1838739Freely accessible. PMID 17108080. 
  50. ^ Cervigne NK, Reis PP, Machado J, Sadikovic B, Bradley G, Galloni NN, Pintilie M, Jurisica I, Gilbert R, Gullane P, Irish J, Kamel-Reid S (2009). "Identification of a microRNA signature associated with progression of leukoplakia to oral carcinoma.". Hum Mol Genet. 18 (24): 4818–29. doi:10.1093/hmg/ddp446. PMID 19776030. 
  51. ^ Schaefer A, Jung M, Mollenkopf HJ, Wagner I, Stephan C, Jentzmik F, Miller K, Lein M, Kristiansen G, Jung K (2010). "Diagnostic and prognostic implications of microRNA profiling in prostate carcinoma.". Int J Cancer. 126 (5): 1166–76. doi:10.1002/ijc.24827. PMID 19676045. 
  52. ^ Szabo DR (Mar 2014). "Analysis of circulating microRNAs in adrenocortical tumors.". Lab Invest. 94 (3): 331–339. doi:10.1038/labinvest.2013.148. PMID 24336071. 
  53. ^ a b Eisenberg I, Eran A, Nishino I, Moggio M, Lamperti C, Amato AA, Lidov HG, Kang PB, North KN, Mitrani-Rosenbaum S, Flanigan KM, Neely LA, Whitney D, Beggs AH, Kohane IS, Kunkel LM (2007). "Distinctive patterns of microRNA expression in primary muscular disorders.". Proc Natl Acad Sci USA. 104 (43): 17016–21. doi:10.1073/pnas.0708115104. PMC 2040449Freely accessible. PMID 17942673. 

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