Mir-17 microRNA precursor family

Last updated
mir-17 microRNA precursor family
RF00051.jpg
Predicted secondary structure and sequence conservation of mir-17
Identifiers
Symbolmir-17
Rfam RF00051
miRBase MI0000071
miRBase family MIPF0000001
Other data
RNA type Gene; miRNA
Domain(s) Eukaryota
GO GO:0035195 GO:0035068
SO SO:0001244
PDB structures PDBe

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]

Contents

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]

Related Research Articles

Myc is a family of regulator genes and proto-oncogenes that code for transcription factors. The Myc family consists of three related human genes: c-myc (MYC), l-myc (MYCL), and n-myc (MYCN). c-myc was the first gene to be discovered in this family, due to homology with the viral gene v-myc.

The Let-7 microRNA precursor was identified from a study of developmental timing in C. elegans, and was later shown to be part of a much larger class of non-coding RNAs termed microRNAs. miR-98 microRNA precursor from human is a let-7 family member. Let-7 miRNAs have now been predicted or experimentally confirmed in a wide range of species (MIPF0000002). miRNAs are initially transcribed in long transcripts called primary miRNAs (pri-miRNAs), which are processed in the nucleus by Drosha and Pasha to hairpin structures of about 70 nucleotide. These precursors (pre-miRNAs) are exported to the cytoplasm by exportin5, where they are subsequently processed by the enzyme Dicer to a ~22 nucleotide mature miRNA. The involvement of Dicer in miRNA processing demonstrates a relationship with the phenomenon of RNA interference.

mir-9/mir-79 microRNA precursor family

The miR-9 microRNA, is a short non-coding RNA gene involved in gene regulation. The mature ~21nt miRNAs are processed from hairpin precursor sequences by the Dicer enzyme. The dominant mature miRNA sequence is processed from the 5' arm of the mir-9 precursor, and from the 3' arm of the mir-79 precursor. The mature products are thought to have regulatory roles through complementarity to mRNA. In vertebrates, miR-9 is highly expressed in the brain, and is suggested to regulate neuronal differentiation. A number of specific targets of miR-9 have been proposed, including the transcription factor REST and its partner CoREST.

mir-16 microRNA precursor family

The miR-16 microRNA precursor family is a group of related small non-coding RNA genes that regulates gene expression. miR-16, miR-15, mir-195 and miR-497 are related microRNA precursor sequences from the mir-15 gene family. This microRNA family appears to be vertebrate specific and its members have been predicted or experimentally validated in a wide range of vertebrate species.

mir-199 microRNA precursor

The miR-199 microRNA precursor is a short non-coding RNA gene involved in gene regulation. miR-199 genes have now been predicted or experimentally confirmed in mouse, human and a further 21 other species. microRNAs are transcribed as ~70 nucleotide precursors and subsequently processed by the Dicer enzyme to give a ~22 nucleotide product. The mature products are thought to have regulatory roles through complementarity to mRNA.

mir-19 microRNA precursor family

There are 89 known sequences today in the microRNA 19 (miR-19) family but it will change quickly. They are found in a large number of vertebrate species. The miR-19 microRNA precursor is a small non-coding RNA molecule that regulates gene expression. Within the human and mouse genome there are three copies of this microRNA that are processed from multiple predicted precursor hairpins:

mir-29 microRNA precursor

The miR-29 microRNA precursor, or pre-miRNA, is a small RNA molecule in the shape of a stem-loop or hairpin. Each arm of the hairpin can be processed into one member of a closely related family of short non-coding RNAs that are involved in regulating gene expression. The processed, or "mature" products of the precursor molecule are known as microRNA (miRNA), and have been predicted or confirmed in a wide range of species.

<span class="mw-page-title-main">MIRH1</span>

Putative microRNA host gene 1 protein is a protein that in humans is encoded by the MIR17HG gene.

mIRN21 Non-coding RNA in the species Homo sapiens

microRNA 21 also known as hsa-mir-21 or miRNA21 is a mammalian microRNA that is encoded by the MIR21 gene.

An oncomir is a microRNA (miRNA) that is associated with cancer. MicroRNAs are short RNA molecules about 22 nucleotides in length. Essentially, miRNAs specifically target certain messenger RNAs (mRNAs) to prevent them from coding for a specific protein. The dysregulation of certain microRNAs (oncomirs) has been associated with specific cancer forming (oncogenic) events. Many different oncomirs have been identified in numerous types of human cancers.

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miR-155 Non-coding RNA in the species Homo sapiens

MiR-155 is a microRNA that in humans is encoded by the MIR155 host gene or MIR155HG. MiR-155 plays a role in various physiological and pathological processes. Exogenous molecular control in vivo of miR-155 expression may inhibit malignant growth, viral infections, and enhance the progression of cardiovascular diseases.

mir-127

mir-127 microRNA is a short non-coding RNA molecule with interesting overlapping gene structure. miR-127 functions to regulate the expression levels of genes involved in lung development, placental formation and apoptosis. Aberrant expression of miR-127 has been linked to different cancers.

mir-200

In molecular biology, the miR-200 microRNA is a short RNA molecule. MicroRNAs function to regulate the expression levels of other genes by binding and cleaving mRNAs or inhibiting translation. The miR-200 family contains miR-200a, miR-200b, miR-200c, miR-141, and miR-429. There is growing evidence to suggest that miR-200 microRNAs are involved in cancer metastasis.

mir-205 Micro RNA involved in the regulation of multiple genes

In molecular biology miR-205 microRNA is a short RNA molecule. MicroRNAs function to regulate the expression levels of other genes by several mechanisms. They are involved in numerous cellular processes, including development, proliferation, and apoptosis. Currently, it is believed that miRNAs elicit their effect by silencing the expression of target genes.

mir-31

miR-31 has been characterised as a tumour suppressor miRNA, with its levels varying in breast cancer cells according to the metastatic state of the tumour. From its typical abundance in healthy tissue is a moderate decrease in non-metastatic breast cancer cell lines, and levels are almost completely absent in mouse and human metastatic breast cancer cell lines. Mir-31-5p has also been observed upregulated in Zinc Deficient rats compared to normal in ESCC and in other types of cancers when using this animal model. There has also been observed a strong encapsulation of tumour cells expressing miR-31, as well as a reduced cell survival rate. miR-31's antimetastatic effects therefore make it a potential therapeutic target for breast cancer. However, these two papers were formally retracted by the authors in 2015.

In molecular biology mir-339 microRNA is a short RNA molecule. MicroRNAs function to regulate the expression levels of other genes by several mechanisms. miR-339-5p expression was associated with overall survival in breast cancer.

In molecular biology mir-885 microRNA is a short RNA molecule. MicroRNAs function to regulate the expression levels of other genes by several mechanisms.

MicroRNA 425 is a microRNA that in humans is encoded by the MIR425 gene.

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.
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  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. Bibcode:2006PNAS..10318680W. 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. Bibcode:2006PLoSO...1..116H. 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. Bibcode:2008PLoSO...3.1719Y. 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. Bibcode:2010PLoSO...512132C. 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.
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  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.
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  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.
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