mir-17 microRNA precursor family
Predicted secondary structure and sequence conservation of mir-17
Identifiers
Symbolmir-17
RfamRF00051
miRBaseMI0000071
miRBase familyMIPF0000001
Other data
RNA typeGene; miRNA
Domain(s)Eukaryota
GOGO:0035195 GO:0035068
SOSO:0001244
PDB structuresPDBe

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] miR-20a detection in human faeces could be a non-invasive screening marker for colorectal cancer.[14]

References

  1. ↑ Tanzer A, Stadler PF (2004). "Molecular evolution of a microRNA cluster". J Mol Biol. 339 (2): 327–35. CiteSeerX 10.1.1.194.1598. 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): 853–858. doi:10.1126/science.1064921. hdl:11858/00-001M-0000-0012-F65F-2. PMID 11679670. S2CID 18101169.
  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. S2CID 682108.
  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. PMC 123250. 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. PMC 1693722. 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. S2CID 2941415.
  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.
  14. ↑ Yau, TO; Wu, CW; Tang, CM; Chen, Y; Fang, J; Dong, Y; Liang, Q; Ng, SS; Chan, FK; Sung, JJ; Yu, J (12 January 2016). "MicroRNA-20a in human faeces as a non-invasive biomarker for colorectal cancer". Oncotarget. 7 (2): 1559–68. doi:10.18632/oncotarget.6403. PMC 4811480. PMID 26621842.

Further reading

  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. PMC 3007123. 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. S2CID 21262482.
  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 S (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): 748–757. doi:10.4161/cbt.10.8.13083. PMID 20703102. S2CID 12028238.
  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. S2CID 24272629.
  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. S2CID 31290845.
  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. PMC 3681296. 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. S2CID 4579895.
  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. S2CID 205786377.
  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.
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  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.
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