mir-22

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.

mir-22
miR-22 microRNA secondary structure and sequence conservation
Identifiers
Symbolmir-22
RfamRF00653
miRBase familyMIPF0000053
NCBI Gene407004
HGNC31599
OMIM612077
Other data
RNA typemicroRNA
Domain(s)Eukaryota; Euteleostomi
PDB structuresPDBe

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]

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] Mir-22 expression was associated with survival in multiple breast cancer datasets.[4]

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).[5] 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.[6]

Possible therapy

Expression of miR-22 can be induced by adding 12-O-Tetradecanoylphorbol-13-acetate (TPA) to HL-60 cells (leukaemia cell line).[7] 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.

gollark: Nonsense, it was obviously gibson.
gollark: And could at the time.
gollark: Also, why would I even bother I can literally see the channel.
gollark: That would be very convoluted and probably get name colors and stuff wrong.
gollark: Also how, since it can't take screenshots.

See also

References

  1. 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.
  2. 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.
  3. 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.
  4. 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.
  5. 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.
  6. 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.
  7. 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.

Further reading

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