mir-17 microRNA precursor family

mir-17 microRNA precursor family
Predicted secondary structure and sequence conservation of mir-17
Identifiers
Symbol mir-17
Rfam RF00051
miRBase MI0000071
miRBase family MIPF0000001
Other data
RNA type Gene; miRNA
Domain(s) Eukaryota
GO 0035195 0035068
SO 0001244

The miR-17 microRNA precursor family are a group of related small non-coding RNA genes called microRNAs that regulate gene expression. The microRNA precursor miR-17 family, includes miR-20a/b, miR-93, and miR-106a/b. With the exception of miR-93, these microRNAs are produced from several microRNA gene clusters, which apparently arose from a series of ancient evolutionary genetic duplication events, and also include members of the miR-19, and miR-25 families.[1] These clusters are transcribed as long non-coding RNA transcripts that are processed to form ~70 nucleotide microRNA precursors, that are subsequently processed by the Dicer enzyme to give a ~22 nucleotide products. The mature microRNA products are thought to regulate expression levels of other genes through complementarity to the 3' UTR of specific target messenger RNA.[2][3]

The paralogous miRNA gene clusters that give rise to miR-17 family microRNAs (miR-17~92, miR-106a~363, and miR-106b~25) have been implicated in a wide variety of malignancies and are sometimes referred to as oncomirs.[4] The oncogenic potential of these non-protein encoding genes was first identified in mouse viral tumorigenesis screens.[5][6][7] In humans, the activating mutations of miR-17~92 have been identified in non-Hodgkin's lymphoma, whereas the miRNA constituents of the clusters are overexpressed in a multiple cancer types.[8][9][10] High level expression of miR-17 family members induces cell proliferation, whereas deletion of the miR-17~92 cluster, in mice, is lethal and causes lung and lymphoid cell developmental defects.[11] In addition, in the nasopharyngeal carcinoma cell line, miR-20a and miR-20b has been shown to target the 3’ UTR of vascular endothelial growth factor (VEGF) and repress the expression of VEGF, which is an important angiogenic factor.[12][13]

References

  1. ↑ Tanzer A, Stadler PF (2004). "Molecular evolution of a microRNA cluster.". J Mol Biol 339: 327–35. doi:10.1016/j.jmb.2004.03.065. PMID 15136036.
  2. ↑ Lagos-Quintana M, Rauhut R, Lendeckel W, Tuschl T (2001). "Identification of novel genes coding for small expressed RNAs.". Science 294 (5543): 853–8. doi:10.1126/science.1064921. PMID 11679670.
  3. ↑ Ambros V (2001). "microRNAs: tiny regulators with great potential.". Cell 107 (7): 823–6. doi:10.1016/S0092-8674(01)00616-X. PMID 11779458.
  4. ↑ Hammond, SM. (Nov 2006). "RNAi, microRNAs, and human disease.". Cancer Chemother Pharmacol. 58 Suppl 1: s63–8. doi:10.1007/s00280-006-0318-2. PMID 17093929.
  5. ↑ Hwang HC, Martins CP, Bronkhorst Y, Randel E, Berns A, Fero ML, Clurman BE (2002). "Identification of oncogenes collaborating with p27Kip1 loss by insertional mutagenesis and high-throughput insertion site analysis.". Proc Natl Acad Sci U S A. 99 (17): 11293–8. doi:10.1073/pnas.162356099. PMID 12151601.
  6. ↑ Wang CL, Wang BB, Bartha G, Li L, Channa N, Klinger M, Killeen N, Wabl M (2006). "Activation of an oncogenic microRNA cistron by provirus integration.". Proc Natl Acad Sci U S A. 103 (49): 18680–4. doi:10.1073/pnas.0609030103. PMID 17121985.
  7. ↑ Landais S, Landry S, Legault P, Rassart E (2007). "Oncogenic potential of the miR-106-363 cluster and its implication in human T-cell leukemia.". Cancer Res. 67 (12): 5699–707. doi:10.1158/0008-5472.CAN-06-4478. PMID 17575136.
  8. ↑ Ota A, Tagawa H, Karnan S, Tsuzuki S, Karpas A, Kira S, Yoshida Y, Seto M (2004). "Identification and characterization of a novel gene, C13orf25, as a target for 13q31-q32 amplification in malignant lymphoma.". Cancer Res. 64 (9): 3087–95. doi:10.1158/0008-5472.CAN-03-3773. PMID 15126345.
  9. ↑ Rinaldi A, Poretti G, Kwee I, Zucca E, Catapano CV, Tibiletti MG, Bertoni F (2007). "Concomitant MYC and microRNA cluster miR-17-92 (C13orf25) amplification in human mantle cell lymphoma.". Leuk Lymphoma. 48 (2): 410–2. doi:10.1080/10428190601059738. PMID 17325905.
  10. ↑ Mendell JT (2008). "miRiad roles for the miR-17-92 cluster in development and disease.". Cell. 133 (2): 217–22. doi:10.1016/j.cell.2008.04.001. PMC 2732113. PMID 18423194.
  11. ↑ Ventura A, Young AG, Winslow MM, Lintault L, Meissner A, Erkeland SJ, Newman J, Bronson RT, Crowley D, Stone JR; et al. (2008). "Targeted deletion reveals essential and overlapping functions of the miR-17~92 family of miRNA clusters.". Cell. 132 (5): 875–86. doi:10.1016/j.cell.2008.02.019. PMC 2323338. PMID 18329372.
  12. ↑ Hua Z, Lv Q, Ye W, Wong CK, Cai G, Gu D, Ji Y, Zhao C, Wang J, Yang BB, Zhang Y (Dec 27, 2006). "MiRNA-directed regulation of VEGF and other angiogenic factors under hypoxia". PLOS ONE 1 (1): e116. doi:10.1371/journal.pone.0000116. PMC 1762435. PMID 17205120.
  13. ↑ Ye W, Lv Q, Wong CK, Hu S, Fu C, Hua Z, Cai G, Li G, Yang BB, Zhang Y (Mar 5, 2008). "The effect of central loops in miRNA:MRE duplexes on the efficiency of miRNA-mediated gene regulation". PLOS ONE 3 (3): e1719. doi:10.1371/journal.pone.0001719. PMC 2248708. PMID 18320040.

Further reading

External links

miRNA precursor families
1-100
101-200
201+
Other
  1. ↑ Dews M, Fox JL, Hultine S, Sundaram P, Wang W, Liu YY, Furth E, Enders GH, El-Deiry W, Schelter JM, Cleary MA, Thomas-Tikhonenko A (2010). "The myc-miR-17~92 axis blunts TGF{beta} signaling and production of multiple TGF{beta}-dependent antiangiogenic factors.". Cancer Res 70 (20): 8233–46. doi:10.1158/0008-5472.CAN-10-2412. PMID 20940405.
  2. ↑ Xiang J, Wu J (2010). "Feud or Friend? The Role of the miR-17-92 Cluster in Tumorigenesis.". Curr Genomics 11 (2): 129–35. doi:10.2174/138920210790886853. PMC 2874222. PMID 20885820.
  3. ↑ Wang Z, Liu M, Zhu H, Zhang W, He S, Hu C, Quan L, Bai J, Xu N (2010). "Suppression of p21 by c-Myc through members of miR-17 family at the post-transcriptional level.". Int J Oncol 37 (5): 1315–21. doi:10.3892/ijo_00000783. PMID 20878079.
  4. ↑ Hong L, Lai M, Chen M, Xie C, Liao R, Kang YJ, Xiao C, Hu WY, Han J, Sun P (2010). "The miR-17-92 cluster of microRNAs confers tumorigenicity by inhibiting oncogene-induced senescence.". Cancer Res 70 (21): 8547–57. doi:10.1158/0008-5472.CAN-10-1938. PMC 2970743. PMID 20851997.
  5. ↑ Osada H, Takahashi T (2010). "Review Article: let-7 and miR-17-92: Small-sized major players in lung cancer development.". Cancer Sci 102 (1): 9–17. doi:10.1111/j.1349-7006.2010.01707.x. PMID 20735434.
  6. ↑ Cox MB, Cairns MJ, Gandhi KS, Carroll AP, Moscovis S, Stewart GJ, Broadley S, Scott RJ, Booth DR, Lechner-Scott J, ANZgene Multiple Sclerosis Genetics Consortium (2010). Jacobson, Steven, ed. "MicroRNAs miR-17 and miR-20a inhibit T cell activation genes and are under-expressed in MS whole blood.". PLoS ONE 5 (8): e12132. doi:10.1371/journal.pone.0012132. PMC 2920328. PMID 20711463.
  7. ↑ Yu J, Ohuchida K, Mizumoto K, Fujita H, Nakata K, Tanaka M (2010). "MicroRNA miR-17-5p is overexpressed in pancreatic cancer, associated with a poor prognosis and involved in cancer cell proliferation and invasion.". Cancer Biol Ther 10 (8): 748. doi:10.4161/cbt.10.8.13083. PMID 20703102.
  8. ↑ Zhuo de X, Niu XH, Chen YC, Xin DQ, Guo YL, Mao ZB (2010). "Vitamin D3 up-regulated protein 1(VDUP1) is regulated by FOXO3A and miR-17-5p at the transcriptional and post-transcriptional levels, respectively, in senescent fibroblasts.". J Biol Chem 285 (41): 31491–501. doi:10.1074/jbc.M109.068387. PMC 2951223. PMID 20656682.
  9. ↑ Kuhnert F, Kuo CJ (2010). "miR-17-92 angiogenesis micromanagement.". Blood 115 (23): 4631–3. doi:10.1182/blood-2010-03-276428. PMID 20538815.
  10. ↑ Li H, Bian C, Liao L, Li J, Zhao RC (2010). "miR-17-5p promotes human breast cancer cell migration and invasion through suppression of HBP1.". Breast Cancer Res Treat 126 (3): 565–575. doi:10.1007/s10549-010-0954-4. PMID 20505989.
  11. ↑ Budde H, Schmitt S, Fitzner D, Opitz L, Salinas-Riester G, Simons M (2010). "Control of oligodendroglial cell number by the miR-17-92 cluster". Development 137 (13): 2127–32. doi:10.1242/dev.050633. PMID 20504959.
  12. ↑ Grillari J, Hackl M, Grillari-Voglauer R (2010). "miR-17-92 cluster: ups and downs in cancer and aging". Biogerontology 11 (4): 501–6. doi:10.1007/s10522-010-9272-9. PMC 2899009. PMID 20437201.
  13. ↑ Wong P, Iwasaki M, Somervaille TC, Ficara F, Carico C, Arnold C, Chen CZ, Cleary ML (2010). "The miR-17-92 microRNA polycistron regulates MLL leukemia stem cell potential by modulating p21 expression". Cancer Res 70 (9): 3833–42. doi:10.1158/0008-5472.CAN-09-3268. PMC 2862107. PMID 20406979.
  14. ↑ Ernst A, Campos B, Meier J, Devens F, Liesenberg F, Wolter M, Reifenberger G, Herold-Mende C, Lichter P, Radlwimmer B (2010). "De-repression of CTGF via the miR-17-92 cluster upon differentiation of human glioblastoma spheroid cultures". Oncogene 29 (23): 3411–22. doi:10.1038/onc.2010.83. PMID 20305691.
  15. ↑ He S, Yang S, Deng G, Liu M, Zhu H, Zhang W, Yan S, Quan L, Bai J, Xu N (2010). "Aurora kinase A induces miR-17-92 cluster through regulation of E2F1 transcription factor". Cell Mol Life Sci 67 (12): 2069–76. doi:10.1007/s00018-010-0340-8. PMID 20300951.
  16. ↑ Olive V, Jiang I, He L (2010). "mir-17-92, a cluster of miRNAs in the midst of the cancer network". Int J Biochem Cell Biol 42 (8): 1348–54. doi:10.1016/j.biocel.2010.03.004. PMID 20227518.
  17. ↑ Tran U, Zakin L, Schweickert A, Agrawal R, Döger R, Blum M, De Robertis EM, Wessely O (2010). "The RNA-binding protein bicaudal C regulates polycystin 2 in the kidney by antagonizing miR-17 activity". Development 137 (7): 1107–16. doi:10.1242/dev.046045. PMC 2835326. PMID 20215348.
  18. ↑ Yang F, Yin Y, Wang F, Wang Y, Zhang L, Tang Y, Sun S (2010). "miR-17-5p Promotes migration of human hepatocellular carcinoma cells through the p38 mitogen-activated protein kinase-heat shock protein 27 pathway". Hepatology 51 (5): 1614–23. doi:10.1002/hep.23566. PMID 20209605.
  19. ↑ Sasaki K, Kohanbash G, Hoji A, Ueda R, McDonald HA, Reinhart TA, Martinson J, Lotze MT, Marincola FM, Wang E, Fujita M, Okada H (2010). "miR-17-92 expression in differentiated T cells - implications for cancer immunotherapy". J Transl Med 8 (1): 17. doi:10.1186/1479-5876-8-17. PMC 2836279. PMID 20167088.
  20. ↑ Lindberg RL, Hoffmann F, Mehling M, Kuhle J, Kappos L (2010). "Altered expression of miR-17-5p in CD4+ lymphocytes of relapsing-remitting multiple sclerosis patients". Eur J Immunol 40 (3): 888–98. doi:10.1002/eji.200940032. PMID 20148420.
  21. ↑ Mi S, Li Z, Chen P, He C, Cao D, Elkahloun A, Lu J, Pelloso LA, Wunderlich M, Huang H, Luo RT, Sun M, He M, Neilly MB, Zeleznik-Le NJ, Thirman MJ, Mulloy JC, Liu PP, Rowley JD, Chen J (2010). "Aberrant overexpression and function of the miR-17-92 cluster in MLL-rearranged acute leukemia". Proc Natl Acad Sci U S A 107 (8): 3710–5. doi:10.1073/pnas.0914900107. PMC 2840429. PMID 20133587.
  22. ↑ Hackl M, Brunner S, Fortschegger K, Schreiner C, Micutkova L, Mück C, Laschober GT, Lepperdinger G, Sampson N, Berger P, Herndler-Brandstetter D, Wieser M, Kühnel H, Strasser A, Rinnerthaler M, Breitenbach M, Mildner M, Eckhart L, Tschachler E, Trost A, Bauer JW, Papak C, Trajanoski Z, Scheideler M, Grillari-Voglauer R, Grubeck-Loebenstein B, Jansen-Dürr P, Grillari J (2010). "miR-17, miR-19b, miR-20a, and miR-106a are down-regulated in human aging". Aging Cell 9 (2): 291–6. doi:10.1111/j.1474-9726.2010.00549.x. PMC 2848978. PMID 20089119.
  23. ↑ van Haaften G, Agami R (2010). "Tumorigenicity of the miR-17-92 cluster distilled". Genes Dev 24 (1): 1–4. doi:10.1101/gad.1887110. PMC 2802185. PMID 20047995.
  24. ↑ Chow TF, Mankaruos M, Scorilas A, Youssef Y, Girgis A, Mossad S, Metias S, Rofael Y, Honey RJ, Stewart R, Pace KT, Yousef GM (2010). "The miR-17-92 cluster is over expressed in and has an oncogenic effect on renal cell carcinoma". J Urol 183 (2): 743–51. doi:10.1016/j.juro.2009.09.086. PMID 20022054.
  25. ↑ Olive V, Bennett MJ, Walker JC, Ma C, Jiang I, Cordon-Cardo C, Li QJ, Lowe SW, Hannon GJ, He L (2009). "miR-19 is a key oncogenic component of mir-17-92". Genes Dev 23 (24): 2839–49. doi:10.1101/gad.1861409. PMC 2800084. PMID 20008935.
  26. ↑ Mu P, Han YC, Betel D, Yao E, Squatrito M, Ogrodowski P, de Stanchina E, D'Andrea A, Sander C, Ventura A (2009). "Genetic dissection of the miR-17~92 cluster of microRNAs in Myc-induced B-cell lymphomas". Genes Dev 23 (24): 2806–11. doi:10.1101/gad.1872909. PMC 2800095. PMID 20008931.
  27. ↑ Guo L, Sun B, Sang F, Wang W, Lu Z (2009). Poon, Art F. Y., ed. "Haplotype distribution and evolutionary pattern of miR-17 and miR-124 families based on population analysis". PLoS ONE 4 (11): e7944. doi:10.1371/journal.pone.0007944. PMC 2775919. PMID 19956752.
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  30. ↑ Yan HL, Xue G, Mei Q, Wang YZ, Ding FX, Liu MF, Lu MH, Tang Y, Yu HY, Sun SH (2009). "Repression of the miR-17-92 cluster by p53 has an important function in hypoxia-induced apoptosis". EMBO J 28 (18): 2719–32. doi:10.1038/emboj.2009.214. PMC 2750010. PMID 19696742.
  31. ↑ Diosdado B, van de Wiel MA, Terhaar Sive Droste JS, Mongera S, Postma C, Meijerink WJ, Carvalho B, Meijer GA (2009). "MiR-17-92 cluster is associated with 13q gain and c-myc expression during colorectal adenoma to adenocarcinoma progression". Br J Cancer 101 (4): 707–14. doi:10.1038/sj.bjc.6605037. PMC 2736819. PMID 19672269.
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  48. ↑ Taguchi A, Yanagisawa K, Tanaka M, Cao K, Matsuyama Y, Goto H, Takahashi T (2008). "Identification of hypoxia-inducible factor-1 alpha as a novel target for miR-17-92 microRNA cluster". Cancer Res 68 (14): 5540–5. doi:10.1158/0008-5472.CAN-07-6460. PMID 18632605.
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  55. ↑ Boggs RM, Moody JA, Long CR, Tsai KL, Murphy KE (2007). "Identification, amplification and characterization of miR-17-92 from canine tissue". Gene 404 (1–2): 25–30. doi:10.1016/j.gene.2007.08.015. PMID 17904311.
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  58. ↑ Matsubara H, Takeuchi T, Nishikawa E, Yanagisawa K, Hayashita Y, Ebi H, Yamada H, Suzuki M, Nagino M, Nimura Y, Osada H, Takahashi T (2007). "Apoptosis induction by antisense oligonucleotides against miR-17-5p and miR-20a in lung cancers overexpressing miR-17-92". Oncogene 26 (41): 6099–105. doi:10.1038/sj.onc.1210425. PMID 17384677.
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