mir-29 microRNA precursor

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mir-29 microRNA precursor
RF00074.jpg
Identifiers
Symbol mir-29
Rfam RF00074
miRBase MI0000087
miRBase family MIPF0000009
Other data
RNA type Gene; miRNA
Domain(s) Eukaryota
GO 0035195 0035068
SO 0001244
PDB structures PDBe

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.[1] 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 (see 'MIPF0000009' in miRBase: the microRNA database[permanent dead link]).

miRNA processing[edit]

Animal miRNAs are first transcribed as a primary miRNA molecule. This "pri-miRNA" may contain one or more precursor hairpins, which are freed from the pri-miRNA by the nuclear enzyme Drosha. The approximately 70 nucleotide precursor hairpin is exported from the nucleus and subsequently processed by the Dicer enzyme to give a mature miRNA that is on average 22 nucleotides long. Either arm of the precursor may yield a mature RNA, although either the 3' (3p) or the 5' (5p) arm is preferentially processed and loaded into the RNA-induced silencing complex (RISC) in most cases. For the miR-29 precursor, the 3' arm of the precursor RNA yields the overwhelmingly predominant product (miR-29 or miR-29-3p), although the 5' arm (miR-29* or miR-29-5p) has also been experimentally verified.

The miR-29 family[edit]

Many mammalian genomes encode four closely related miR-29 precursors that are transcribed in two transcriptional units. For example, human miR-29a and miR-29b-1 are processed from an intron of a long non-coding transcript (LOC646329) from chromosome 7. miR-29b-2 (identical in sequence to miR-29b-1) and miR-29c are co-transcribed from chromosome 1. The three main mature miRNAs processed from these precursors are known as has-miR-29a, has-miR-29b, and has-miR-29c.

Survival analysis across three independent datasets shows that hsa-miR-29c is associated with survival in breast cancer.[2]

Targets of miR-29[edit]

The mature products are thought to exert regulatory roles by binding with partial complementarity to microRNA recognition elements (MREs) in the 3' untranslated region (3' UTR) of target transcripts. Experimental evidence suggests that putative targets of mature miR-29 products include the following:

Recently, in an attempt to identify targets at global level using Quantitative proteomics - SILAC approach, VDAC1 and VDAC2 were identified as targets of miR-29a in HEK293T cells.[8]

References[edit]

  1. ^ Ambros V (Dec 2001). "microRNAs: tiny regulators with great potential". Cell. 107 (7): 823–6. doi:10.1016/S0092-8674(01)00616-X. PMID 11779458. 
  2. ^ Lánczky, András; Nagy, Ádám; Bottai, Giulia; Munkácsy, Gyöngyi; Szabó, András; Santarpia, Libero; Győrffy, Balázs (2016-12-01). "miRpower: a web-tool to validate survival-associated miRNAs utilizing expression data from 2178 breast cancer patients". Breast Cancer Research and Treatment. 160 (3): 439–446. doi:10.1007/s10549-016-4013-7. ISSN 1573-7217. PMID 27744485. 
  3. ^ Mott JL, Kobayashi S, Bronk SF, Gores GJ (Sep 2007). "mir-29 regulates Mcl-1 protein expression and apoptosis". Oncogene. 26 (42): 6133–40. doi:10.1038/sj.onc.1210436. PMC 2432524Freely accessible. PMID 17404574. 
  4. ^ Pekarsky Y, Santanam U, Cimmino A, Palamarchuk A, Efanov A, Maximov V, Volinia S, Alder H, Liu CG, Rassenti L, Calin GA, Hagan JP, Kipps T, Croce CM (Dec 2006). "Tcl1 expression in chronic lymphocytic leukemia is regulated by miR-29 and miR-181". Cancer Research. 66 (24): 11590–3. doi:10.1158/0008-5472.CAN-06-3613. PMID 17178851. 
  5. ^ Fabbri M, Garzon R, Cimmino A, Liu Z, Zanesi N, Callegari E, Liu S, Alder H, Costinean S, Fernandez-Cymering C, Volinia S, Guler G, Morrison CD, Chan KK, Marcucci G, Calin GA, Huebner K, Croce CM (Oct 2007). "MicroRNA-29 family reverts aberrant methylation in lung cancer by targeting DNA methyltransferases 3A and 3B". Proceedings of the National Academy of Sciences of the United States of America. 104 (40): 15805–10. doi:10.1073/pnas.0707628104. PMC 2000384Freely accessible. PMID 17890317. 
  6. ^ Gebeshuber CA, Zatloukal K, Martinez J (Apr 2009). "miR-29a suppresses tristetraprolin, which is a regulator of epithelial polarity and metastasis". EMBO Reports. 10 (4): 400–5. doi:10.1038/embor.2009.9. PMC 2672883Freely accessible. PMID 19247375. 
  7. ^ Sanduja S, Blanco FF, Dixon DA (2011). "The roles of TTP and BRF proteins in regulated mRNA decay". Wiley Interdisciplinary Reviews. RNA. 2 (1): 42–57. doi:10.1002/wrna.28. PMC 3030256Freely accessible. PMID 21278925. 
  8. ^ Bargaje R, Gupta S, Sarkeshik A, Park R, Xu T, Sarkar M, Halimani M, Roy SS, Yates J, Pillai B (2012). "Identification of novel targets for miR-29a using miRNA proteomics". PLOS ONE. 7 (8): e43243. doi:10.1371/journal.pone.0043243. PMC 3428309Freely accessible. PMID 22952654. 

Further reading[edit]

  • Zhang X, Zhao X, Fiskus W, Lin J, Lwin T, Rao R, Zhang Y, Chan JC, Fu K, Marquez VE, Chen-Kiang S, Moscinski LC, Seto E, Dalton WS, Wright KL, Sotomayor E, Bhalla K, Tao J (Oct 2012). "Coordinated silencing of MYC-mediated miR-29 by HDAC3 and EZH2 as a therapeutic target of histone modification in aggressive B-Cell lymphomas". Cancer Cell. 22 (4): 506–23. doi:10.1016/j.ccr.2012.09.003. PMID 23079660. 

External links[edit]