Mir-9/mir-79 microRNA precursor family

Last updated
mir-9
RF00237.jpg
miR-9 microRNA secondary structure and sequence conservation.
Identifiers
Symbolmir-9
Rfam RF00237
miRBase family MIPF0000014
HGNC 31641
OMIM 611186
Other data
RNA type microRNA
Domain(s) Eukaryota;
PDB structures PDBe

The miR-9 microRNA (homologous to miR-79), 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. [1] In vertebrates, miR-9 is highly expressed in the brain, and is suggested to regulate neuronal differentiation. [2] A number of specific targets of miR-9 have been proposed, including the transcription factor REST and its partner CoREST. [3]

Contents

Species distribution

miR-9 has been identified in Drosophila (MI0000129), [4] mouse (MI0000720) and human (MI0000466), [5] and the related miR-79 in C. elegans (MI0000050) [6] and Drosophila melanogaster (MI0000374). [7]

Role in disease

microRNAs have been implicated in human cancer in a number of studies. It has been shown that human miR-9 expression levels are reduced in many breast cancer samples due to hypermethylation an epigenetic modification. [8] Hildebrandt et al. show that two genes encoding for has-miR-9 are significantly hypermethylated in clear cell renal carcinoma tumours. [9]

Related Research Articles

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-15 microRNA precursor family

The miR-15 microRNA precursor family is made up of small non-coding RNA genes that regulate gene expression. The family includes the related mir-15a and mir-15b sequences, as well as miR-16-1, miR-16-2, miR-195 and miR-497. These six highly conserved miRNAs are clustered on three separate chromosomes. In humans miR-15a and miR-16 are clustered within 0.5 kilobases at chromosome position 13q14. This region has been found to be the most commonly affected in chronic lymphocytic leukaemia (CLL), with deletions of the entire region in more than half of cases. Both miR-15a and miR-16 are thus frequently deleted or down-regulated in CLL samples with 13q14 deletions; occurring in more than two thirds of CLL cases. The expression of miR-15a is associated with survival in triple negative breast cancer.

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-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. 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.

mir-196 microRNA precursor family

miR-196 is a non-coding RNA called a microRNA that has been shown to be expressed in humans and mice. miR-196 appears to be a vertebrate specific microRNA and has now been predicted or experimentally confirmed in a wide range of vertebrate species. In many species the miRNA appears to be expressed from intergenic regions in HOX gene clusters. The hairpin precursors are predicted based on base pairing and cross-species conservation—their extents are not known. In this case the mature sequence is excised from the 5' arm of the hairpin.

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-1 microRNA precursor family

The miR-1 microRNA precursor is a small micro RNA that regulates its target protein's expression in the cell. microRNAs are transcribed as ~70 nucleotide precursors and subsequently processed by the Dicer enzyme to give products at ~22 nucleotides. In this case the mature sequence comes from the 3' arm of the precursor. The mature products are thought to have regulatory roles through complementarity to mRNA. In humans there are two distinct microRNAs that share an identical mature sequence, and these are called miR-1-1 and miR-1-2.

mir-30 microRNA precursor

miR-30 microRNA precursor is a small non-coding RNA that regulates gene expression. Animal microRNAs are transcribed as pri-miRNA of varying length which in turns are processed in the nucleus by Drosha into ~70 nucleotide stem-loop precursor called pre-miRNA and subsequently processed by the Dicer enzyme to give a mature ~22 nucleotide product. In this case the mature sequence comes from both the 3' (miR-30) and 5' (mir-97-6) arms of the precursor. The products are thought to have regulatory roles through complementarity to mRNA.

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.

mir-96 microRNA

miR-96 microRNA precursor is a small non-coding RNA that regulates gene expression. microRNAs are transcribed as ~80 nucleotide precursors and subsequently processed by the Dicer enzyme to give a ~23 nucleotide products. In this case the mature sequence comes from the 5′ arm of the precursor. The mature products are thought to have regulatory roles through complementarity to mRNA.

mir-126

In molecular biology mir-126 is a short non-coding RNA molecule. MicroRNAs function to regulate the expression levels of other genes by several pre- and post-transcription mechanisms.

mir-143 RNA molecule

In molecular biology mir-143 microRNA is a short RNA molecule. MicroRNAs function to regulate the expression levels of other genes by several mechanisms. mir–143 is highly conserved in vertebrates. mir-143 is thought be involved in cardiac morphogenesis but has also been implicated in cancer.

mir-145 Non-coding RNA in the species Homo sapiens

In molecular biology, mir-145 microRNA is a short RNA molecule that in humans is encoded by the MIR145 gene. MicroRNAs function to regulate the expression levels of other genes by several mechanisms.

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-22

In molecular biology mir-22 microRNA is a short RNA molecule. MicroRNAs are an abundant class of molecules, approximately 22 nucleotides in length, which can post-transcriptionally regulate gene expression by binding to the 3' UTR of mRNAs expressed in a cell.

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.

mir-221 microRNA

In molecular biology, mir-221 microRNA is a short RNA molecule. MicroRNAs function to regulate the expression levels of other genes by several mechanisms.

In molecular biology mir-365 microRNA is a short RNA molecule. MicroRNAs function to regulate the expression levels of other genes by several mechanisms.

References

  1. ↑ Ambros V (2001). "microRNAs: tiny regulators with great potential". Cell. 107 (7): 823–6. doi: 10.1016/S0092-8674(01)00616-X . PMID   11779458.
  2. ↑ Delaloy C, Liu L, Lee JA, Su H, Shen F, Yang GY, Young WL, Ivey KN, Gao FB (2010). "MicroRNA-9 coordinates proliferation and migration of human embryonic stem cell-derived neural progenitors". Cell Stem Cell. 6 (4): 323–35. doi:10.1016/j.stem.2010.02.015. PMC   2851637 . PMID   20362537.
  3. ↑ Packer AN, Xing Y, Harper SQ, Jones L, Davidson BL (2008). "The bifunctional microRNA miR-9/miR-9* regulates REST and CoREST and is downregulated in Huntington's disease". J Neurosci. 28 (53): 14341–6. doi:10.1523/JNEUROSCI.2390-08.2008. PMC   3124002 . PMID   19118166.
  4. ↑ 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. hdl: 11858/00-001M-0000-0012-F65F-2 . PMID   11679670. S2CID   18101169.
  5. ↑ Lagos-Quintana M, Rauhut R, Yalcin A, Meyer J, Lendeckel W, Tuschl T (2002). "Identification of tissue-specific microRNAs from mouse". Curr. Biol. 12 (9): 735–9. doi:10.1016/S0960-9822(02)00809-6. hdl: 11858/00-001M-0000-0010-94EF-7 . PMID   12007417. S2CID   7901788.
  6. ↑ Lau NC, Lim LP, Weinstein EG, Bartel DP (2001). "An abundant class of tiny RNAs with probable regulatory roles in Caenorhabditis elegans". Science. 294 (5543): 858–62. doi:10.1126/science.1065062. PMID   11679671. S2CID   43262684.
  7. ↑ Sempere LF, Sokol NS, Dubrovsky EB, Berger EM, Ambros V (2003). "Temporal regulation of microRNA expression in Drosophila melanogaster mediated by hormonal signals and broad-Complex gene activity". Dev. Biol. 259 (1): 9–18. doi: 10.1016/S0012-1606(03)00208-2 . PMID   12812784.
  8. ↑ Lehmann U, Hasemeier B, Christgen M, et al. (2007). "Epigenetic inactivation of microRNA gene hsa-mir-9-1 in human breast cancer". The Journal of Pathology. 214 (1): 17–24. doi:10.1002/path.2251. PMID   17948228. S2CID   22024957.
  9. ↑ Hildebrandt MA, Gu J, Lin J, Ye Y, Tan W, Tamboli P, Wood CG, Wu X (2010). "Hsa-miR-9 methylation status is associated with cancer development and metastatic recurrence in patients with clear cell renal cell carcinoma". Oncogene. 29 (42): 5724–8. doi: 10.1038/onc.2010.305 . PMID   20676129.

Further reading

  1. ↑ Kutty RK, Samuel W, Jaworski C, Duncan T, Nagineni CN, Raghavachari N, Wiggert B, Redmond TM (2010). "MicroRNA expression in human retinal pigment epithelial (ARPE-19) cells: increased expression of microRNA-9 by N-(4-hydroxyphenyl)retinamide". Mol Vis. 16: 1475–86. PMC   2925906 . PMID   20806079.
  2. ↑ Delaloy C, Gao FB (2010). "A new role for microRNA-9 in human neural progenitor cells". Cell Cycle. 9 (15): 2913–4. doi:10.4161/cc.9.15.12699. PMC   5764704 . PMID   20676037.
  3. ↑ Laneve P, Gioia U, Andriotto A, Moretti F, Bozzoni I, Caffarelli E (2010). "A minicircuitry involving REST and CREB controls miR-9-2 expression during human neuronal differentiation". Nucleic Acids Res. 38 (20): 6895–905. doi:10.1093/nar/gkq604. PMC   2978373 . PMID   20624818.
  4. ↑ Almeida MI, Reis RM, Calin GA (2010). "MYC-microRNA-9-metastasis connection in breast cancer". Cell Res. 20 (6): 603–4. doi: 10.1038/cr.2010.70 . hdl: 1822/67519 . PMID   20502442.
  5. ↑ Uchida N (2010). "MicroRNA-9 controls a migratory mechanism in human neural progenitor cells". Cell Stem Cell. 6 (4): 294–6. doi: 10.1016/j.stem.2010.03.010 . PMID   20362531.
  6. ↑ Wang K, Long B, Zhou J, Li PF (2010). "miR-9 and NFATc3 regulate myocardin in cardiac hypertrophy". J Biol Chem. 285 (16): 11903–12. doi: 10.1074/jbc.M109.098004 . PMC   2852927 . PMID   20177053.
  7. ↑ Khew-Goodall Y, Goodall GJ (2010). "Myc-modulated miR-9 makes more metastases". Nat Cell Biol. 12 (3): 209–11. doi: 10.1038/ncb0310-209 . PMID   20173743.
  8. ↑ Ma L, Young J, Prabhala H, Pan E, Mestdagh P, Muth D, Teruya-Feldstein J, Reinhardt F, Onder TT, Valastyan S, Westermann F, Speleman F, Vandesompele J, Weinberg RA (2010). "miR-9, a MYC/MYCN-activated microRNA, regulates E-cadherin and cancer metastasis". Nat Cell Biol. 12 (3): 247–56. doi:10.1038/ncb2024. PMC   2845545 . PMID   20173740.
  9. ↑ Wan HY, Guo LM, Liu T, Liu M, Li X, Tang H (2010). "Regulation of the transcription factor NF-kappaB1 by microRNA-9 in human gastric adenocarcinoma". Mol Cancer. 9 (1): 16. doi: 10.1186/1476-4598-9-16 . PMC   2835654 . PMID   20102618.
  10. ↑ Guo LM, Pu Y, Han Z, Liu T, Li YX, Liu M, Li X, Tang H (2009). "MicroRNA-9 inhibits ovarian cancer cell growth through regulation of NF-kappaB1". FEBS J. 276 (19): 5537–46. doi:10.1111/j.1742-4658.2009.07237.x. PMID   19702828. S2CID   19354709.
  11. ↑ Tan HX, Wang Q, Chen LZ, Huang XH, Chen JS, Fu XH, Cao LQ, Chen XL, Li W, Zhang LJ (2010). "MicroRNA-9 reduces cell invasion and E-cadherin secretion in SK-Hep-1 cell". Med Oncol. 27 (3): 654–60. doi:10.1007/s12032-009-9264-2. PMID   19572217. S2CID   195246235.
  12. ↑ Hsu PY, Deatherage DE, Rodriguez BA, Liyanarachchi S, Weng YI, Zuo T, Liu J, Cheng AS, Huang TH (2009). "Xenoestrogen-induced epigenetic repression of microRNA-9-3 in breast epithelial cells". Cancer Res. 69 (14): 5936–45. doi:10.1158/0008-5472.CAN-08-4914. PMC   2855843 . PMID   19549897.
  13. ↑ Luo H, Zhang H, Zhang Z, Zhang X, Ning B, Guo J, Nie N, Liu B, Wu X (2009). "Down-regulated miR-9 and miR-433 in human gastric carcinoma". J Exp Clin Cancer Res. 28 (1): 82. doi: 10.1186/1756-9966-28-82 . PMC   2739520 . PMID   19531230.
  14. ↑ Denli AM, Cao X, Gage FH (2009). "miR-9 and TLX: chasing tails in neural stem cells". Nat Struct Mol Biol. 16 (4): 346–7. doi:10.1038/nsmb0409-346. PMID   19343066. S2CID   9788995.
  15. ↑ Zhao C, Sun G, Li S, Shi Y (2009). "A feedback regulatory loop involving microRNA-9 and nuclear receptor TLX in neural stem cell fate determination". Nat Struct Mol Biol. 16 (4): 365–71. doi:10.1038/nsmb.1576. PMC   2667220 . PMID   19330006.
  16. ↑ Bazzoni F, Rossato M, Fabbri M, Gaudiosi D, Mirolo M, Mori L, Tamassia N, Mantovani A, Cassatella MA, Locati M (2009). "Induction and regulatory function of miR-9 in human monocytes and neutrophils exposed to proinflammatory signals". Proc Natl Acad Sci U S A. 106 (13): 5282–7. doi: 10.1073/pnas.0810909106 . PMC   2664036 . PMID   19289835.
  17. ↑ Packer AN, Xing Y, Harper SQ, Jones L, Davidson BL (2008). "The bifunctional microRNA miR-9/miR-9* regulates REST and CoREST and is downregulated in Huntington's disease". J Neurosci. 28 (53): 14341–6. doi:10.1523/JNEUROSCI.2390-08.2008. PMC   3124002 . PMID   19118166.
  18. ↑ Shibata M, Kurokawa D, Nakao H, Ohmura T, Aizawa S (2008). "MicroRNA-9 modulates Cajal-Retzius cell differentiation by suppressing Foxg1 expression in mouse medial pallium". J Neurosci. 28 (41): 10415–21. doi:10.1523/JNEUROSCI.3219-08.2008. PMC   6671033 . PMID   18842901.
  19. ↑ Chao TF, Zhang Y, Yan XQ, Yin B, Gong YH, Yuan JG, Qiang BQ, Peng XZ (2008). "[MiR-9 regulates the expression of CBX7 in human glioma]". Zhongguo Yi Xue Ke Xue Yuan Xue Bao. 30 (3): 268–74. PMID   18686603.
  20. ↑ Pietrzykowski AZ, Friesen RM, Martin GE, Puig SI, Nowak CL, Wynne PM, Siegelmann HT, Treistman SN (2008). "Posttranscriptional regulation of BK channel splice variant stability by miR-9 underlies neuroadaptation to alcohol". Neuron. 59 (2): 274–87. doi:10.1016/j.neuron.2008.05.032. PMC   2714263 . PMID   18667155.
  21. ↑ Nass D, Rosenwald S, Meiri E, Gilad S, Tabibian-Keissar H, Schlosberg A, Kuker H, Sion-Vardy N, Tobar A, Kharenko O, Sitbon E, Lithwick Yanai G, Elyakim E, Cholakh H, Gibori H, Spector Y, Bentwich Z, Barshack I, Rosenfeld N (2009). "MiR-92b and miR-9/9* are specifically expressed in brain primary tumors and can be used to differentiate primary from metastatic brain tumors". Brain Pathol. 19 (3): 375–83. doi:10.1111/j.1750-3639.2008.00184.x. PMC   2728890 . PMID   18624795.
  22. ↑ Delaloy C, Gao FB (2008). "microRNA-9 multitasking near organizing centers". Nat Neurosci. 11 (6): 625–6. doi:10.1038/nn0608-625. PMC   4446695 . PMID   18506136.
  23. ↑ Leucht C, Stigloher C, Wizenmann A, Klafke R, Folchert A, Bally-Cuif L (2008). "MicroRNA-9 directs late organizer activity of the midbrain-hindbrain boundary". Nat Neurosci. 11 (6): 641–8. doi:10.1038/nn.2115. PMID   18454145. S2CID   7031726.
  24. ↑ Laios A, O'Toole S, Flavin R, Martin C, Kelly L, Ring M, Finn SP, Barrett C, Loda M, Gleeson N, D'Arcy T, McGuinness E, Sheils O, Sheppard B, O' Leary J (2008). "Potential role of miR-9 and miR-223 in recurrent ovarian cancer". Mol Cancer. 7 (1): 35. doi: 10.1186/1476-4598-7-35 . PMC   2383925 . PMID   18442408.
  25. ↑ Lehmann U, Hasemeier B, Christgen M, Müller M, Römermann D, Länger F, Kreipe H (2008). "Epigenetic inactivation of microRNA gene hsa-mir-9-1 in human breast cancer". J Pathol. 214 (1): 17–24. doi:10.1002/path.2251. PMID   17948228. S2CID   22024957.
  26. ↑ Plaisance V, Abderrahmani A, Perret-Menoud V, Jacquemin P, Lemaigre F, Regazzi R (2006). "MicroRNA-9 controls the expression of Granuphilin/Slp4 and the secretory response of insulin-producing cells". J Biol Chem. 281 (37): 26932–42. doi: 10.1074/jbc.M601225200 . PMID   16831872.
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