mir-16
miR-16 microRNA secondary structure and sequence conservation.
Identifiers
Symbolmir-16
RfamRF00254
miRBase familyMIPF0000006
HGNC31545
OMIM609704
Other data
RNA typemicroRNA
Domain(s)Eukaryota;
PDB structuresPDBe

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 (MIPF0000006).

Background

The human miR-16 precursor was discovered through detailed expression profile and Karyotype analyses of patients by Calin and colleagues.[1] Karyotyping of chromosome structures from individuals with B-cell chronic lymphocytic leukaemias (B-CLL) found that more than half have alterations in the 13q14 region.[1][2] Deletions of this well characterised 1 megabase region of the genome[3][4] was also observed in approximately 50% of mantle cell lymphoma, up to 40% of multiple myeloma, and 60% of prostate cancers.[5] Comprehensive screenings of the region at the time did not provide consistent evidence of involvement from any of the known genes at the time.[3][4][6][7][8][9][10] Using CD5+ B-lymphocytes,[11] which is known to accumulate with B-CLL progression, the minimal region lost from 13q14 region was scrutinised for regulatory elements.[1] Publicly available sequence databases were used to identify a gene cluster which encodes the homologue to the human miR15 and miR16 from the Caenorhabditis elegans.[12][13][14]

Gene targets

In the original publication which identified the action of miR15 and miR16 in the development of B-CLL, Calin and colleagues proposed that miR16 could be the targets with imperfect base pairing for 14 genes.[1] Increased CD5+ B-lymphocytes in CLL suggests the miR16 may be involved in cellular differentiation.[1] In animal models single-stranded microRNA species act by binding to imperfect mRNA complements, typically to the 3' UTR,[15][16] although targets have also been observed in the coding sequence of the mRNA.[15][17] Downregulation of miR16 (as well as miR15) was observed in diffuse large B-cell lymphoma.[18] miR16 has been shown to bind to a nine base pair to a complementary sequence in the 3' UTR region of BCL2, which is an anti-apoptotic gene involved in an evolutionarily conserved pathway in programmed cell death.[19] In the nasopharyngeal carcinoma cell line, miR-16 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.[20][21]

Clinical relevance

Altered expression of microRNA-16 has been observed in cancer,[22][23][24] including malignancies of the breast,[25] colon[26][27], brain[28][29] , lung[30], lymphatic system[1][18][31][32], ovaries[33], pancreas[34] , prostate[35] and stomach.[36] This difference in expression levels can be used distinguish between cancerous and healthy tissues and to determine clinical prognosis.[27][37][38] The fact that pathology is associated with a different expression profile has led to the proposal that disease specific biomarkers can provide potential targets for directed clinical intervention.[39] More recently, there is evidence that in colorectal cancer that the efficacy of treatment with the monoclonal antibody cetuximab can be assessed by the expression pattern of colorectal carcinoma after therapy.[40]

miR-16 and miR-15a are clustered within a 0.5 kbp region in Chromosome 13 (13q14) in humans, a chromosomal region shown to be deleted or down-regulated in approximately more than half of B-CLL,[1] the most prevalent form of leukemia in adults.[41] Carcinogenesis is a gradual process, involving multiple genetic mutations, thus every patient with malignancy presents with a heterogeneous population of cells. The fact that mir-16 microRNA loss is observed in a large proportion of cells indicates the change occurred early in cancer development[23] and a target for therapeutic intervention.

References

  1. 1 2 3 4 5 6 7 Calin GA, Dumitru CD, Shimizu M, Bichi R, Zupo S, Noch E, Aldler H, Rattan S, Keating M, Rai K, Rassenti L, Kipps T, Negrini M, Bullrich F, Croce CM (2002). "Frequent deletions and down-regulation of micro-RNA genes miR15 and miR16 at 13q14 in chronic lymphocytic leukemia". Proc Natl Acad Sci USA. 99 (24): 15524–15529. Bibcode:2002PNAS...9915524C. doi:10.1073/pnas.242606799. PMC 137750. PMID 12434020.
  2. ↑ Coll-Mulet L, Gil J (2009). "Genetic alterations in chronic lymphocytic leukaemia". Clin Transl Oncol. 11 (4): 194–198. doi:10.1007/s12094-009-0340-z. PMID 19380295. S2CID 36669052.
  3. 1 2 Bullrich F, Fujii H, Calin G, Mabuchi H, Negrini M, Pekarsky Y, Rassenti L, Alder H, Reed JC, Keating MJ, Kipps TJ, Croce C, M. (2001). "Characterization of the 13q14 tumor suppressor locus in CLL: identification of ALT1, an alternative splice variant of the LEU2 gene". Cancer Res. 61 (18): 6640–6648. PMID 11559527.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  4. 1 2 Migliazza A, Bosch F, Komatsu H, Cayanis E, Martinotti S, Toniato E, Guccione E, Qu X, Chien M, Murty VV, Gaidano G, Inghirami G, Zhang P, Fischer S, Kalachikov SM, Russo J, Edelman I, Efstratiadis A, Dalla-Favera R (2001). "Nucleotide sequence, transcription map, and mutation analysis of the 13q14 chromosomal region deleted in B-cell chronic lymphocytic leukemia". Blood. 97 (7): 2098–2104. doi:10.1182/blood.V97.7.2098. PMID 11264177.
  5. ↑ Dong JT, Boyd JC, Frierson HF Jr (2001). "Loss of heterozygosity at 13q14 and 13q21 in high grade, high stage prostate cancer". Prostate. 49 (3): 166–171. doi:10.1002/pros.1131. PMID 11746261. S2CID 40075043.
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  7. ↑ Mabuchi H, Fujii H, Calin G, Alder H, Negrini M, Rassenti L, Kipps TJ, Bullrich F, Croce CM (2001). "Cloning and characterization of CLLD6, CLLD7, and CLLD8, novel candidate genes for leukemogenesis at chromosome 13q14, a region commonly deleted in B-cell chronic lymphocytic leukemia". Cancer Res. 61 (7): 2870–2877. PMID 11306461.
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Further reading

[1] [2] [3] [4] [5] [6] [7] [8] [9] [10] [11] [12] [13] [14] [15] [16] [17] [18] [19] [20] [21] [22] [23] [24] [25] [26] [27] [28]

  1. ↑ Baudry A, Mouillet-Richard S, Schneider B, Launay JM, Kellermann O (2010). "miR-16 targets the serotonin transporter: a new facet for adaptive responses to antidepressants". Science. 329 (5998): 1537–41. Bibcode:2010Sci...329.1537B. doi:10.1126/science.1193692. PMID 20847275. S2CID 7835219.
  2. ↑ Zhang X, Wan G, Mlotshwa S, Vance V, Berger FG, Chen H, Lu X (2010). "Oncogenic Wip1 phosphatase is inhibited by miR-16 in the DNA damage signaling pathway". Cancer Res. 70 (18): 7176–86. doi:10.1158/0008-5472.CAN-10-0697. PMC 2940956. PMID 20668064.
  3. ↑ Maccani MA, Avissar-Whiting M, Banister CE, McGonnigal B, Padbury JF, Marsit CJ (2010). "Maternal cigarette smoking during pregnancy is associated with downregulation of miR-16, miR-21 and miR-146a in the placenta". Epigenetics. 5 (7): 583–9. doi:10.4161/epi.5.7.12762. PMC 2974801. PMID 20647767.
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  5. ↑ Xu F, Zhang X, Lei Y, Liu X, Liu Z, Tong T, Wang W (2010). "Loss of repression of HuR translation by miR-16 may be responsible for the elevation of HuR in human breast carcinoma". J Cell Biochem. 111 (3): 727–34. doi:10.1002/jcb.22762. PMID 20626035. S2CID 19458784.
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  24. ↑ Calin GA, Cimmino A, Fabbri M, Ferracin M, Wojcik SE, Shimizu M, Taccioli C, Zanesi N, Garzon R, Aqeilan RI, Alder H, Volinia S, Rassenti L, Liu X, Liu CG, Kipps TJ, Negrini M, Croce CM (2008). "MiR-15a and miR-16-1 cluster functions in human leukemia". Proc Natl Acad Sci U S A. 105 (13): 5166–71. Bibcode:2008PNAS..105.5166C. doi:10.1073/pnas.0800121105. PMC 2278188. PMID 18362358.
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  26. ↑ Raveche ES, Salerno E, Scaglione BJ, Manohar V, Abbasi F, Lin YC, Fredrickson T, Landgraf P, Ramachandra S, Huppi K, Toro JR, Zenger VE, Metcalf RA, Marti GE (2007). "Abnormal microRNA-16 locus with synteny to human 13q14 linked to CLL in NZB mice". Blood. 109 (12): 5079–86. doi:10.1182/blood-2007-02-071225. PMC 1890829. PMID 17351108.
  27. ↑ Linsley PS, Schelter J, Burchard J, Kibukawa M, Martin MM, Bartz SR, Johnson JM, Cummins JM, Raymond CK, Dai H, Chau N, Cleary M, Jackson AL, Carleton M, Lim L (2007). "Transcripts targeted by the microRNA-16 family cooperatively regulate cell cycle progression". Mol Cell Biol. 27 (6): 2240–52. doi:10.1128/MCB.02005-06. PMC 1820501. PMID 17242205.
  28. ↑ Bottoni A, Piccin D, Tagliati F, Luchin A, Zatelli MC, degli Uberti EC (2005). "miR-15a and miR-16-1 down-regulation in pituitary adenomas". J Cell Physiol. 204 (1): 280–5. doi:10.1002/jcp.20282. PMID 15648093. S2CID 39337781.
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