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miR-27 is a family of microRNA precursors found in animals, including humans. MicroRNAs are typically transcribed as ~70 nucleotide precursors and subsequently processed by the Dicer enzyme to give a ~22 nucleotide product. The excised region or, mature product, of the miR-27 precursor is the microRNA mir-27.
Herpesvirus saimiri expresses several non-coding RNAs (HSURs) which have been found to significantly reduce the level of mir-27 in a host cell. It has been proposed that miR-27 operates together with miR-23 and mir-24 in a co-operative cluster.
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miR-27 is a family of microRNA precursors found in animals, including humans.[1] MicroRNAs are typically transcribed as ~70 nucleotide precursors and subsequently processed by the Dicer enzyme to give a ~22 nucleotide product.[2] The excised region or, mature product, of the miR-27 precursor is the microRNA mir-27.
Herpesvirus saimiri expresses several non-coding RNAs (HSURs) which have been found to significantly reduce the level of mir-27 in a host cell.[3] It has been proposed that miR-27 operates together with miR-23 and mir-24 in a co-operative cluster.[4]
[edit] Regulation of adipocyte differentiation
miR-27 is one of a number of microRNAs implicated in cholesterol homeostasis and fatty acid metabolism.[5] The miR-27 gene family has been shown to be downregulated during the differentiation of adipocytes. miR-27 overexpression inhibits adipocyte formation when overexpressed, acting by blocking the expression of two main regulators of adipogenesis.[6] MicroRNAs miR-27a and -27b have been found to negatively regulate adipocyte differentiation through regulation of the peroxisome proliferator-activated receptor gamma (PPARγ) post-transcriptionally, as well as C/EBP alpha in the case of miR-27b.[7] miR-27 can be identified both as an adipogenic inhibitor and as playing an important role in the development of obesity.[6]
[edit] Wnt signalling pathway
miR-27 is an activator of the Wnt signalling pathway, affecting the differentiation of mesenchymal stem cells into osteoblasts.[8] miR-27 has been found to target and inhibit gene expression of the adenomatous polyposis coli (APC) protein, enabling it to regulate osteoblast differentiation. Expression levels of miR-27 are positively correlated with beta-catenin,[9] a key protein in Wnt signalling. There is activation of Wnt signalling through nuclear accumulation of this protein, which is in response to inhibition of the beta-catenin destruction complex. This in turn is brought about by APC inhibition of miR-27.[9]
[edit] Cancer Regulation
miR-27 is known to regulate components involved in numerous types of cancer, including breast[10][11] and ovarian.[12] miR-27a has been identified as an oncogenic microRNA and, specifically, is highly expressed in breast cancer cells. Inhibition of miR-27 by antisense molecules decreases cell proliferation.[13] Antisense RNA directed against miR-27a has been shown to decrease the percentage of cells in S phase whilst also increasing those in the G2-M phase.[14]
The FOXO (Forkhead Box O) gene sub-family encodes tumour-suppressive transcription factors that regulate multiple aspects of cell cycle progression and survival. FOXO1 protein expression is down-regulated in breast tumour tissue samples; miR-27a has been identified as one of three miRNAS (along with miR-96 and miR-182) which directly target FOXO1 and regulate its endogenous expression. Suppression of miR-27a results in a FOXO1 protein increase and a consequent cell number decrease.[14]
[edit] References
- ^ Landgraf, P; Rusu, M, Sheridan, R, Sewer, A, Iovino, N, Aravin, A, Pfeffer, S, Rice, A et al. (2007 Jun 29). "A mammalian microRNA expression atlas based on small RNA library sequencing.". Cell 129 (7): 1401–14. doi:10.1016/j.cell.2007.04.040. PMC 2681231. PMID 17604727. //www.ncbi.nlm.nih.gov/pmc/articles/PMC2681231/.
- ^ Ambros, V (2001). "microRNAs: tiny regulators with great potential". Cell 107 (7): 823–826. doi:10.1016/S0092-8674(01)00616-X. PMID 11779458.
- ^ Cazalla, D; Yario, T, Steitz, JA (2010 Jun 18). "Down-regulation of a host microRNA by a Herpesvirus saimiri noncoding RNA.". Science 328 (5985): 1563–6. doi:10.1126/science.1187197. PMC 3075239. PMID 20558719. //www.ncbi.nlm.nih.gov/pmc/articles/PMC3075239/.
- ^ Chhabra, R; Dubey, R, Saini, N (2010 Sep 3). "Cooperative and individualistic functions of the microRNAs in the miR-23a~27a~24-2 cluster and its implication in human diseases.". Molecular cancer 9: 232. doi:10.1186/1476-4598-9-232. PMC 2940846. PMID 20815877. //www.ncbi.nlm.nih.gov/pmc/articles/PMC2940846/.
- ^ Fernández-Hernando, C; Suárez, Y, Rayner, KJ, Moore, KJ (2011 Apr). "MicroRNAs in lipid metabolism.". Current opinion in lipidology 22 (2): 86–92. doi:10.1097/MOL.0b013e3283428d9d. PMC 3096067. PMID 21178770. //www.ncbi.nlm.nih.gov/pmc/articles/PMC3096067/.
- ^ a b Lin Q, Gao Z, Alarcon RM, Ye J, Yun Z (2009). "A role of miR-27 in the regulation of adipogenesis.". FEBS J 276 (8): 2348–58. PMID 19348006. http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19348006.
- ^ Kim SY, Kim AY, Lee HW, Son YH, Lee GY, Lee JW et al. (2010). "miR-27a is a negative regulator of adipocyte differentiation via suppressing PPARgamma expression.". Biochem Biophys Res Commun 392 (3): 323–8. doi:10.1016/j.bbrc.2010.01.012. PMID 20060380. http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20060380.
- ^ Wang, T; Xu, Z (2010 Nov 12). "miR-27 promotes osteoblast differentiation by modulating Wnt signaling.". Biochemical and Biophysical Research Communications 402 (2): 186–9. doi:10.1016/j.bbrc.2010.08.031. PMID 20708603.
- ^ a b Wang T, Xu Z (2010). "miR-27 promotes osteoblast differentiation by modulating Wnt signaling.". Biochem Biophys Res Commun 402 (2): 186–9. doi:10.1016/j.bbrc.2010.08.031. PMID 20708603. http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20708603.
- ^ Li, X; Mertens-Talcott, SU, Zhang, S, Kim, K, Ball, J, Safe, S (2010 Jun). "MicroRNA-27a Indirectly Regulates Estrogen Receptor {alpha} Expression and Hormone Responsiveness in MCF-7 Breast Cancer Cells.". Endocrinology 151 (6): 2462–73. doi:10.1210/en.2009-1150. PMC 2875816. PMID 20382698. //www.ncbi.nlm.nih.gov/pmc/articles/PMC2875816/.
- ^ Guttilla, IK; White, BA (2009 Aug 28). "Coordinate regulation of FOXO1 by miR-27a, miR-96, and miR-182 in breast cancer cells.". The Journal of Biological Chemistry 284 (35): 23204–16. doi:10.1074/jbc.M109.031427. PMC 2749094. PMID 19574223. //www.ncbi.nlm.nih.gov/pmc/articles/PMC2749094/.
- ^ Kontorovich, T; Levy, A, Korostishevsky, M, Nir, U, Friedman, E (2010 Aug 1). "Single nucleotide polymorphisms in miRNA binding sites and miRNA genes as breast/ovarian cancer risk modifiers in Jewish high-risk women.". International Journal of Cancer. Journal International Du Cancer 127 (3): 589–97. doi:10.1002/ijc.25065. PMID 19950226.
- ^ Mertens-Talcott SU, Chintharlapalli S, Li X, Safe S (2007). "The oncogenic microRNA-27a targets genes that regulate specificity protein transcription factors and the G2-M checkpoint in MDA-MB-231 breast cancer cells.". Cancer Res 67 (22): 11001–11. doi:10.1158/0008-5472.CAN-07-2416. PMID 18006846. http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18006846.
- ^ a b Guttilla IK, White BA (2009). "Coordinate regulation of FOXO1 by miR-27a, miR-96, and miR-182 in breast cancer cells.". J Biol Chem 284 (35): 23204–16. doi:10.1074/jbc.M109.031427. PMC 2749094. PMID 19574223. //www.ncbi.nlm.nih.gov/pmc/articles/PMC2749094/.
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