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
Identifiers
Symbolmir-17
RfamRF00051
miRBaseMI0000071
miRBase familyMIPF0000001
Other data
RNA typeGene; miRNA
Domain(s)Eukaryota
GOGO:0035195 GO:0035068
SOSO:0001244
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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  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.
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  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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