| Community annotation |
This text is a summary paragraph taken from the Wikipedia
entry entitled Mir-22. miRBase and Rfam
are facilitating community annotation of microRNA families and entries in Wikipedia. Read more ...
The text in this section is taken from the free, online
encyclopedia, Wikipedia. Anyone can edit a Wikipedia page. We hope
that experts on particular microRNA sequences will use the links to
Wikipedia below to edit the annotation of individual microRNAs, to add
information about function, evolution, discovery, and literature
references, for example. Any changes that you make will be visible in
Wikipedia immediately, and in miRBase within 24 hours.
Editing Wikipedia entries is straightforward. If you haven't
edited a page before, you might like to take a look at the following
Wikipedia help pages:
You can also create new pages at Wikipedia about microRNA families
that do not currently have specific entries there. Please let us know
if you do, so we can incorporate your annotation into miRBase, and
create the appropriate links from miRBase entries to the relevant
Wikipedia pages.
Please note, we're not responsible for the content of Wikipedia pages.
You can read more about miRBase, Wikipedia and community annotation on this blog post.
Please email us for
help or with comments about this community annotation initiative.
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.
Show Wikipedia entry
View @ Wikipedia
Edit Wikipedia entry
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.
[edit] Origins
Mir-22 was originally identified in HeLa cells (an immortal cell line derived from cervical cancer cells), but was later found to be ubiquitously expressed in various tissues.[1] The gene encoding miR-22 is found on the short arm of chromosome 17, in a minimal loss of heterozygosity region. It is highly conserved across many vertebrate species, including chimp, mouse, rat, dog and horse. This level of conservation suggests functional importance. MiR-22 was previously identified as having a role in erythrocyte maturation.[2]
[edit] Role in cancer
The deregulation of many miRNAs has been shown to have a role in oncogenesis. Mir-22 was found to be over-expressed in prostate cancer but down-regulated in breast cancer, cholangiocarcinoma, multiple myeloma and hepatocellular carcinoma.[3]
[edit] Targets
Specifically, miR-22 can function as a tumour suppressor. One known target is histone deacetylase 4 (HDAC4), which is known to have a critical role in cancer development. Mir-22 also targets Myc Binding Protein (MYCBP).[4] This prevents transcription of c-Myc target genes by silencing c-MYCBP. However, c-Myc also inhibits expression of miR-22 in a positive feedback loop. When this spirals out of control, it can cause uncontrolled cell proliferation.[5]
[edit] Possible therapy
Expression of miR-22 can be induced by adding 12-O-Tetradecanoylphorbol-13-acetate (TPA) to HL-60 cells (leukaemia cell line).[6] The enforced expression causes the growth of cancer cells to slow down. This means that miR-22 could be a potential target for cancer therapies.
[edit] See also
[edit] References
- ^ Xiong J, Yu D, Wei N, Fu H, Cai T, Huang Y, Wu C, Zheng X, Du Q, Lin D, Liang Z (2010). "An estrogen receptor alpha suppressor, microRNA-22, is downregulated in estrogen receptor alpha-positive human breast cancer cell lines and clinical samples.". FEBS J 277 (7): 1684–94. doi:10.1111/j.1742-4658.2010.07594.x. PMID 20180843.
- ^ Choong ML, Yang HH, McNiece I (April 2007). "MicroRNA expression profiling during human cord blood-derived CD34 cell erythropoiesis". Exp. Hematol. 35 (4): 551–64. doi:10.1016/j.exphem.2006.12.002. PMID 17379065.
- ^ Zhang J, Yang Y, Yang T, Liu Y, Li A, Fu S, Wu M, Pan Z, Zhou W (2010). "microRNA-22, downregulated in hepatocellular carcinoma and correlated with prognosis, suppresses cell proliferation and tumourigenicity". Br J Cancer 103 (8): 1215–20. doi:10.1038/sj.bjc.6605895. PMC 2967065. PMID 20842113. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2967065.
- ^ Xiong J, Du Q, Liang Z (2010). "Tumor-suppressive microRNA-22 inhibits the transcription of E-box-containing c-Myc target genes by silencing c-Myc binding protein". Oncogene 29 (35): 4980–8. doi:10.1038/onc.2010.241. PMID 20562918.
- ^ Cole MD, McMahon SB (May 1999). "The Myc oncoprotein: a critical evaluation of transactivation and target gene regulation". Oncogene 18 (19): 2916–24. doi:10.1038/sj.onc.1202748. PMID 10378688.
- ^ Ting Y, Medina DJ, Strair RK, Schaar DG (2010). "Differentiation-associated miR-22 represses Max expression and inhibits cell cycle progression". Biochem Biophys Res Commun 394 (3): 606–11. doi:10.1016/j.bbrc.2010.03.030. PMID 20214878.
[edit] Further reading
- ^ Li J, Liang S, Yu H, Zhang J, Ma D, Lu X (2010). "An inhibitory effect of miR-22 on cell migration and invasion in ovarian cancer". Gynecol Oncol 119 (3): 543–8. doi:10.1016/j.ygyno.2010.08.034. PMID 20869762.
- ^ Bar N, Dikstein R (2010). Ulrich, Henning. ed. "miR-22 forms a regulatory loop in PTEN/AKT pathway and modulates signaling kinetics". PLoS ONE 5 (5): e10859. doi:10.1371/journal.pone.0010859. PMC 2877705. PMID 20523723. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2877705.
- ^ Liu L, Jiang Y, Zhang H, Greenlee AR, Yu R, Yang Q (2010). "miR-22 functions as a micro-oncogene in transformed human bronchial epithelial cells induced by anti-benzo[a]pyrene-7,8-diol-9,10-epoxide". Toxicol in Vitro 24 (4): 1168–75. doi:10.1016/j.tiv.2010.02.016. PMID 20170724.
- ^ Pandey DP, Picard D (2009). "miR-22 inhibits estrogen signaling by directly targeting the estrogen receptor alpha mRNA". Mol Cell Biol 29 (13): 3783–90. doi:10.1128/MCB.01875-08. PMC 2698751. PMID 19414598. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2698751.
[edit] External links
|
