mir-17 microRNA precursor family

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]

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
GO0035195 0035068
SO0001244
PDB structuresPDBe

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
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  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. 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.
  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.
  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.
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