Biology:mir-16 microRNA precursor family

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mir-16
RF00254.jpg
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 ([1]). 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, [citation needed] up to 40% of multiple myeloma, [citation needed] 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. ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 "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. 2002. doi:10.1073/pnas.242606799. PMID 12434020. Bibcode: 2002PNAS...9915524C. 
  2. ↑ "Genetic alterations in chronic lymphocytic leukaemia.". Clin Transl Oncol 11 (4): 194– 198. 2009. doi:10.1007/s12094-009-0340-z. PMID 19380295. 
  3. ↑ 3.0 3.1 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. http://cancerres.aacrjournals.org/content/61/18/6640.full. 
  4. ↑ 4.0 4.1 "Nucleotide sequence, transcription map, and mutation analysis of the 13q14 chromosomal region deleted in B-cell chronic lymphocytic leukemia.". Blood 97 (7): 2098– 2104. 2001. doi:10.1182/blood.V97.7.2098. PMID 11264177. 
  5. ↑ "Loss of heterozygosity at 13q14 and 13q21 in high grade, high stage prostate cancer.". Prostate 49 (3): 166– 171. 2001. doi:10.1002/pros.1131. PMID 11746261. 
  6. ↑ "Cloning of two candidate tumor suppressor genes within a 10 kb region on chromosome 13q14, frequently deleted in chronic lymphocytic leukemia.". Oncogene 15 (20): 2463– 2473. 1997. doi:10.1038/sj.onc.1201643. PMID 9395242. 
  7. ↑ "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. 2001. PMID 11306461. http://cancerres.aacrjournals.org/content/61/7/2870.full. 
  8. ↑ "Comprehensive analysis of a large genomic sequence at the putative B-cell chronic lymphocytic leukaemia (B-CLL) tumour suppresser gene locus.". Mutat Res 458 (3–4): 55–70. 2001. doi:10.1016/S0027-5107(01)00219-6. PMID 11691637. 
  9. ↑ "B-cell neoplasia associated gene with multiple splicing (BCMS): the candidate B-CLL gene on 13q14 comprises more than 560 kb covering all critical regions". Hum Mol Genet 10 (12): 1275– 1285. 2001. doi:10.1093/hmg/10.12.1275. PMID 11406609. 
  10. ↑ "Deletion analysis of chromosome 13q14.3 and characterisation of an alternative splice form of LEU1 in B cell chronic lymphocytic leukemia". Leukemia 16 (17): 1267– 1275. 2002. doi:10.1038/sj.leu.2402551. PMID 12094250. 
  11. ↑ "B-cell chronic lymphocytic leukemia: a bird of a different feather". J Clin Oncol 17 (1): 399– 408. 1999. doi:10.1200/JCO.1999.17.1.399. PMID 10458259. 
  12. ↑ "Identification of novel genes coding for small expressed RNAs". Science 294 (5543): 853– 858. 2001. doi:10.1126/science.1064921. PMID 11679670. Bibcode: 2001Sci...294..853L. 
  13. ↑ "An abundant class of tiny RNAs with probable regulatory roles in Caenorhabditis elegans". Science 294 (5543): 858– 862. 2001. doi:10.1126/science.1065062. PMID 11679671. Bibcode: 2001Sci...294..858L. 
  14. ↑ "An extensive class of small RNAs in Caenorhabditis elegans". Science 294 (5543): 862– 864. 2001. doi:10.1126/science.1065329. PMID 11679672. Bibcode: 2001Sci...294..862L. 
  15. ↑ 15.0 15.1 "Conserved seed pairing, often flanked by adenosines, indicates that thousands of human genes are microRNA targets". Cell 120 (1): 15– 20. 2005. doi:10.1016/j.cell.2004.12.035. PMID 15652477. 
  16. ↑ "Systematic discovery of regulatory motifs in human promoters and 3' UTRs by comparison of several mammals". Nature 434 (7031): 338– 345. 2005. doi:10.1038/nature03441. PMID 15735639. Bibcode: 2005Natur.434..338X. 
  17. ↑ "MicroRNAs to Nanog, Oct4 and Sox2 coding regions modulate embryonic stem cell differentiation". Nature 455 (7216): 1124– 1128. 2008. doi:10.1038/nature07299. PMID 18806776. Bibcode: 2008Natur.455.1124T. 
  18. ↑ 18.0 18.1 "Accumulation of miR-155 and BIC RNA in human B-cell lymphoma". Proc Natl Acad Sci U S A 102 (10): 3627–3632. 2004. doi:10.1073/pnas.0500613102. PMID 15738415. 
  19. ↑ "miR-15 and miR-16 induce apoptosis by targeting BCL2". Proc Natl Acad Sci U S A 102 (39): 13944– 13949. 2005. doi:10.1073/pnas.0506654102. PMID 16166262. Bibcode: 2005PNAS..10213944C. 
  20. ↑ "MiRNA-directed regulation of VEGF and other angiogenic factors under hypoxia". PLOS ONE 1 (1): e116. 27 December 2006. doi:10.1371/journal.pone.0000116. PMID 17205120. Bibcode: 2006PLoSO...1..116H. 
  21. ↑ "The effect of central loops in miRNA:MRE duplexes on the efficiency of miRNA-mediated gene regulation". PLOS ONE 3 (3): e1719. 5 March 2008. doi:10.1371/journal.pone.0001719. PMID 18320040. Bibcode: 2008PLoSO...3.1719Y. 
  22. ↑ "MicroRNA expression profiles classify human cancers". Nature 435 (7043): 834–838. 2005. doi:10.1038/nature03702. PMID 15944708. Bibcode: 2005Natur.435..834L. 
  23. ↑ 23.0 23.1 Croce CM. (2009). "Causes and consequences of microRNA dysregulation in cancer". Nat Rev Genet 10 (10): 704–714. doi:10.1038/nrg2634. PMID 19763153. 
  24. ↑ "Human microRNA genes are frequently located at fragile sites and genomic regions involved in cancers". Proc Natl Acad Sci U S A 101 (9): 2999– 3004. 2004. doi:10.1073/pnas.0307323101. PMID 14973191. Bibcode: 2004PNAS..101.2999C. 
  25. ↑ "Downregulation of the tumor-suppressor miR-16 via progestin-mediated oncogenic signaling contributes to breast cancer development". Breast Cancer Res 14 (3): R77. 2012. doi:10.1186/bcr3187. PMID 22583478. 
  26. ↑ "Reduced accumulation of specific microRNAs in colorectal neoplasia". Mol Cancer Res 1 (12): 882–891. 2003. PMID 14573789. http://mcr.aacrjournals.org/content/1/12/882.long. 
  27. ↑ 27.0 27.1 "MicroRNA expression profiles associated with prognosis and therapeutic outcome in colon adenocarcinoma". JAMA 299 (4): 425– 436. 2008. doi:10.1001/jama.299.4.425. PMID 18230780. 
  28. ↑ "Extensive modulation of a set of microRNAs in primary glioblastoma". Biochem Biophys Res Commun 334 (4): 1351– 1358. 2005. doi:10.1016/j.bbrc.2005.07.030. PMID 16039986. 
  29. ↑ "MicroRNA-21 is an antiapoptotic factor in human glioblastoma cells". Cancer Res 65 (14): 6029– 6033. 2007. doi:10.1158/0008-5472.CAN-05-0137. PMID 16024602. http://cancerres.aacrjournals.org/content/65/14/6029.full. 
  30. ↑ "Reduced expression of the let-7 microRNAs in human lung cancers in association with shortened postoperative survival". Cancer Res 64 (11): 3753–3756. 2004. doi:10.1158/0008-5472.CAN-04-0637. PMID 15172979. http://cancerres.aacrjournals.org/content/64/11/3753.long. 
  31. ↑ "High expression of precursor microRNA-155/BIC RNA in children with Burkitt's lymphoma". Genes Chromosomes Cancer 39 (2): 167–169. 2004. doi:10.1002/gcc.10316. PMID 14695998. 
  32. ↑ "Identification and characterization of a novel gene, C13orf25, as a target for 13q31-q32 amplification in malignant Lymphoma". Cancer Res 64 (9): 3087– 3095. 2004. doi:10.1158/0008-5472.CAN-03-3773. PMID 15126345. http://cancerres.aacrjournals.org/content/64/9/3087.long. 
  33. ↑ "MicroRNA signatures in human ovarian cancer". Cancer Res 67 (8): 8699– 8707. 2007. doi:10.1158/0008-5472.CAN-07-1936. PMID 17875710. http://cancerres.aacrjournals.org/content/67/18/8699.long. 
  34. ↑ "MicroRNA expression patterns to differentiate pancreatic adenocarcinoma from normal pancreas and chronic pancreatitis". JAMA 297 (17): 1901– 1908. 2007. doi:10.1001/jama.297.17.1901. PMID 17473300. 
  35. ↑ "The miR-15a-miR-16-1 cluster controls prostate cancer by targeting multiple oncogenic activities". Nat Med 14 (11): 1271– 1277. 2008. doi:10.1038/nm.1880. PMID 18931683. 
  36. ↑ "MicroRNA signatures in human ovarian cancer". Cancer Cell 13 (3): 272– 286. 2008. doi:10.1016/j.ccr.2008.02.013. PMID 18328430. 
  37. ↑ "Unique microRNA molecular profiles in lung cancer diagnosis and prognosis". Cancer Cell 9 (3): 189– 198. 2006. doi:10.1016/j.ccr.2006.01.025. PMID 16530703. 
  38. ↑ "A MicroRNA signature associated with prognosis and progression in chronic lymphocytic leukemia". N Engl J Med 353 (17): 1793– 1801. 2005. doi:10.1056/NEJMoa050995. PMID 16251535. 
  39. ↑ Cho WC. (2010). "A MicroRNA signature associated with prognosis and progression in chronic lymphocytic leukemia". Expert Opin Ther Targets 14 (10): 1005– 1008. doi:10.1517/14728222.2010.522399. PMID 20854177. 
  40. ↑ "Specific alterations of microRNA transcriptome and global network structure in colorectal carcinoma after cetuximab treatment". Mol Cancer Ther 14 (10): 1005– 1008. 2010. doi:10.1158/1535-7163.MCT-10-0137. PMID 20881268. http://mct.aacrjournals.org/content/early/2010/09/22/1535-7163.MCT-10-0137. 
  41. ↑ Döhner H; Stilgenbauer S. Benner A; Leupolt E; Krober A; Bullinger L; Dohner K; Bentz M; Lichter P. (2000). "Genomic Aberrations and Survival in Chronic Lymphocytic Leukemia". N Engl J Med 343 (26): 1910–1916. doi:10.1056/NEJM200012283432602. PMID 11136261. 

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]

External links



  1. ↑ "miR-16 targets the serotonin transporter: a new facet for adaptive responses to antidepressants". Science 329 (5998): 1537–41. 2010. doi:10.1126/science.1193692. PMID 20847275. Bibcode: 2010Sci...329.1537B. 
  2. ↑ "Oncogenic Wip1 phosphatase is inhibited by miR-16 in the DNA damage signaling pathway". Cancer Res 70 (18): 7176–86. 2010. doi:10.1158/0008-5472.CAN-10-0697. PMID 20668064. 
  3. ↑ "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. 2010. doi:10.4161/epi.5.7.12762. PMID 20647767. 
  4. ↑ "MicroRNA mir-16 is anti-proliferative in enterocytes and exhibits diurnal rhythmicity in intestinal crypts". Exp Cell Res 316 (20): 3512–21. 2010. doi:10.1016/j.yexcr.2010.07.007. PMID 20633552. 
  5. ↑ "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. 2010. doi:10.1002/jcb.22762. PMID 20626035. 
  6. ↑ "MicroRNA-16 targets amyloid precursor protein to potentially modulate Alzheimer's-associated pathogenesis in SAMP8 mice". Neurobiol Aging 33 (3): 522–534. 2010. doi:10.1016/j.neurobiolaging.2010.04.034. PMID 20619502. 
  7. ↑ "Curcumin reduces the expression of Bcl-2 by upregulating miR-15a and miR-16 in MCF-7 cells". Med Oncol 27 (4): 1114–8. 2009. doi:10.1007/s12032-009-9344-3. PMID 19908170. 
  8. ↑ "MiR-15a and MiR-16 control Bmi-1 expression in ovarian cancer". Cancer Res 69 (23): 9090–5. 2009. doi:10.1158/0008-5472.CAN-09-2552. PMID 19903841. 
  9. ↑ "Effects of upregulated expression of microRNA-16 on biological properties of culture-activated hepatic stellate cells". Apoptosis 14 (11): 1331–40. 2009. doi:10.1007/s10495-009-0401-3. PMID 19784778. 
  10. ↑ Williams, Simon, ed (2009). "Investigating the targets of MIR-15a and MIR-16-1 in patients with chronic lymphocytic leukemia (CLL)". PLOS ONE 4 (9): e7169. doi:10.1371/journal.pone.0007169. PMID 19779621. Bibcode: 2009PLoSO...4.7169H. 
  11. ↑ "Systemic delivery of synthetic microRNA-16 inhibits the growth of metastatic prostate tumors via downregulation of multiple cell-cycle genes". Mol Ther 18 (1): 181–7. 2010. doi:10.1038/mt.2009.207. PMID 19738602. 
  12. ↑ "DLEU2, frequently deleted in malignancy, functions as a critical host gene of the cell cycle inhibitory microRNAs miR-15a and miR-16-1". Exp Cell Res 315 (17): 2941–52. 2009. doi:10.1016/j.yexcr.2009.07.001. PMID 19591824. 
  13. ↑ "miR-15a and miR-16 are implicated in cell cycle regulation in a Rb-dependent manner and are frequently deleted or down-regulated in non-small cell lung cancer". Cancer Res 69 (13): 5553–9. 2009. doi:10.1158/0008-5472.CAN-08-4277. PMID 19549910. 
  14. ↑ "miR-15a and miR-16-1 in cancer: discovery, function and future perspectives". Cell Death Differ 17 (2): 215–20. 2010. doi:10.1038/cdd.2009.69. PMID 19498445. 
  15. ↑ "Epigallocatechin gallate up-regulation of miR-16 and induction of apoptosis in human cancer cells". J Nutr Biochem 21 (2): 140–6. 2010. doi:10.1016/j.jnutbio.2008.12.003. PMID 19269153. 
  16. ↑ "Two new miR-16 targets: caprin-1 and HMGA1, proteins implicated in cell proliferation". Biol Cell 101 (9): 511–24. 2009. doi:10.1042/BC20080213. PMID 19250063. 
  17. ↑ "miR-15b and miR-16 are implicated in activation of the rat hepatic stellate cell: An essential role for apoptosis". J Hepatol 50 (4): 766–78. 2009. doi:10.1016/j.jhep.2008.11.025. PMID 19232449. 
  18. ↑ "Prognostic value of miR-16 expression in childhood acute lymphoblastic leukemia relationships to normal and malignant lymphocyte proliferation". Leuk Res 33 (9): 1217–23. 2009. doi:10.1016/j.leukres.2008.12.015. PMID 19195700. 
  19. ↑ "The VEGF IRESes are differentially susceptible to translation inhibition by miR-16". RNA 15 (2): 249–54. 2009. doi:10.1261/rna.1301109. PMID 19144909. 
  20. ↑ "Distinct roles of heterogeneous nuclear ribonuclear protein K and microRNA-16 in cyclooxygenase-2 RNA stability induced by S100b, a ligand of the receptor for advanced glycation end products". J Biol Chem 283 (52): 36221–33. 2008. doi:10.1074/jbc.M806322200. PMID 18854308. 
  21. ↑ "miR-16 family induces cell cycle arrest by regulating multiple cell cycle genes". Nucleic Acids Res 36 (16): 5391–404. 2008. doi:10.1093/nar/gkn522. PMID 18701644. 
  22. ↑ "Truncation in CCND1 mRNA alters miR-16-1 regulation in mantle cell lymphoma". Blood 112 (3): 822–9. 2008. doi:10.1182/blood-2008-03-142182. PMID 18483394. 
  23. ↑ "miR-15b and miR-16 modulate multidrug resistance by targeting BCL2 in human gastric cancer cells". Int J Cancer 123 (2): 372–9. 2008. doi:10.1002/ijc.23501. PMID 18449891. 
  24. ↑ "MiR-15a and miR-16-1 cluster functions in human leukemia". Proc Natl Acad Sci U S A 105 (13): 5166–71. 2008. doi:10.1073/pnas.0800121105. PMID 18362358. Bibcode: 2008PNAS..105.5166C. 
  25. ↑ "Murine models of chronic lymphocytic leukaemia: role of microRNA-16 in the New Zealand Black mouse model". Br J Haematol 139 (5): 645–57. 2007. doi:10.1111/j.1365-2141.2007.06851.x. PMID 17941951. 
  26. ↑ "Abnormal microRNA-16 locus with synteny to human 13q14 linked to CLL in NZB mice". Blood 109 (12): 5079–86. 2007. doi:10.1182/blood-2007-02-071225. PMID 17351108. 
  27. ↑ "Transcripts targeted by the microRNA-16 family cooperatively regulate cell cycle progression". Mol Cell Biol 27 (6): 2240–52. 2007. doi:10.1128/MCB.02005-06. PMID 17242205. 
  28. ↑ "miR-15a and miR-16-1 down-regulation in pituitary adenomas". J Cell Physiol 204 (1): 280–5. 2005. doi:10.1002/jcp.20282. PMID 15648093. 
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