MIR489: Difference between revisions

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{{Infobox_gene}}
{{Infobox_gene}}
 
'''MicroRNA 489''' is a miRNA that in humans is encoded by the MIR489 [[gene]].<ref name="entrez">{{cite web | title = Entrez Gene: MicroRNA 489 | url = https://www.ncbi.nlm.nih.gov/gene/574442 }}</ref>
'''MicroRNA 489''' is a miRNA that in humans is encoded by the MIR489 [[gene]].
<ref name="entrez">
{{cite web
| title = Entrez Gene: MicroRNA 489
| url = https://www.ncbi.nlm.nih.gov/gene/574442
| accessdate = 2016-12-05
}}</ref>


==Function==
==Function==


microRNAs (miRNAs) are short (20-24 nt) non-coding RNAs that are involved in post-transcriptional regulation of gene expression in multicellular organisms by affecting both the stability and translation of mRNAs. miRNAs are transcribed by RNA polymerase II as part of capped and polyadenylated primary transcripts (pri-miRNAs) that can be either protein-coding or non-coding. The primary transcript is cleaved by the Drosha ribonuclease III enzyme to produce an approximately 70-nt stem-loop precursor miRNA (pre-miRNA), which is further cleaved by the cytoplasmic Dicer ribonuclease to generate the mature miRNA and antisense miRNA star (miRNA*) products. The mature miRNA is incorporated into a RNA-induced silencing complex (RISC), which recognizes target mRNAs through imperfect base pairing with the miRNA and most commonly results in translational inhibition or destabilization of the target mRNA. The RefSeq represents the predicted microRNA stem-loop.
microRNAs (miRNAs) are short (20-24 nt) non-coding RNAs that are involved in post-transcriptional regulation of gene expression in multicellular organisms by affecting both the stability and translation of mRNAs. miRNAs are transcribed by RNA polymerase II as part of capped and polyadenylated primary transcripts (pri-miRNAs) that can be either protein-coding or non-coding. The primary transcript is cleaved by the Drosha ribonuclease III enzyme to produce an approximately 70-nt stem-loop precursor miRNA (pre-miRNA), which is further cleaved by the cytoplasmic Dicer ribonuclease to generate the mature miRNA and antisense miRNA star (miRNA*) products. The mature miRNA is incorporated into a RNA-induced silencing complex (RISC), which recognizes target mRNAs through imperfect base pairing with the miRNA and most commonly results in translational inhibition or destabilization of the target mRNA. The RefSeq represents the predicted microRNA stem-loop. miR-489 acts as tumor suppressor miRNA in breast cancer by inhibiting various oncogenic signaling pathway. It has been demonstrated miR-489 target HER2 and LAPTM4b by directly binding to their 3'UTR. Role of miR-489 has been studied in autochatothus MMTV-Her2 mouse model.<ref name="pmid26918448">{{cite journal | vauthors = Patel Y, Shah N, Lee JS, Markoutsa E, Jie C, Liu S, Botbyl R, Reisman D, Xu P, Chen H | title = A novel double-negative feedback loop between miR-489 and the HER2-SHP2-MAPK signaling axis regulates breast cancer cell proliferation and tumor growth | journal = Oncotarget | volume = 7 | issue = 14 | pages = 18295–308 | date = April 2016 | pmid = 26918448 | pmc = 4951289 | doi = 10.18632/oncotarget.7577 }}</ref>


== References ==
== References ==
{{reflist}}
{{reflist}}


== Further reading ==
== Further reading ==
{{refbegin | 2}}
{{refbegin | 2}}
*{{cite journal |vauthors=Kikkawa N, Hanazawa T, Fujimura L, Nohata N, Suzuki H, Chazono H, Sakurai D, Horiguchi S, Okamoto Y, Seki N |title=miR-489 is a tumour-suppressive miRNA target PTPN11 in hypopharyngeal squamous cell carcinoma (HSCC) |journal=Br. J. Cancer |volume=103 |issue=6 |pages=877–84 |year=2010 |pmid=20700123 |pmc=2966617 |doi=10.1038/sj.bjc.6605811 |url=}}
*{{cite journal |vauthors=Kikkawa N, Hanazawa T, Fujimura L, Nohata N, Suzuki H, Chazono H, Sakurai D, Horiguchi S, Okamoto Y, Seki N |title=miR-489 is a tumour-suppressive miRNA target PTPN11 in hypopharyngeal squamous cell carcinoma (HSCC) |journal=Br. J. Cancer |volume=103 |issue=6 |pages=877–84 |year=2010 |pmid=20700123 |pmc=2966617 |doi=10.1038/sj.bjc.6605811 |url=}}
*{{cite journal |vauthors=Wu H, Xiao Z, Zhang H, Wang K, Liu W, Hao Q |title=MiR-489 modulates cisplatin resistance in human ovarian cancer cells by targeting Akt3 |journal=Anticancer Drugs |volume=25 |issue=7 |pages=799–809 |year=2014 |pmid=24686007 |doi=10.1097/CAD.0000000000000107 |url=}}
*{{cite journal |vauthors=Wu H, Xiao Z, Zhang H, Wang K, Liu W, Hao Q |title=MiR-489 modulates cisplatin resistance in human ovarian cancer cells by targeting Akt3 |journal=Anticancer Drugs |volume=25 |issue=7 |pages=799–809 |year=2014 |pmid=24686007 |doi=10.1097/CAD.0000000000000107 |url=}}
*{{cite journal |vauthors=Jiang L, He D, Yang D, Chen Z, Pan Q, Mao A, Cai Y, Li X, Xing H, Shi M, Chen Y, Bruce IC, Wang T, Jin L, Qi X, Hua D, Jin J, Ma X |title=MiR-489 regulates chemoresistance in breast cancer via epithelial mesenchymal transition pathway |journal=FEBS Lett. |volume=588 |issue=11 |pages=2009–15 |year=2014 |pmid=24786471 |doi=10.1016/j.febslet.2014.04.024 |url=}}
*{{cite journal |vauthors=Jiang L, He D, Yang D, Chen Z, Pan Q, Mao A, Cai Y, Li X, Xing H, Shi M, Chen Y, Bruce IC, Wang T, Jin L, Qi X, Hua D, Jin J, Ma X |title=MiR-489 regulates chemoresistance in breast cancer via epithelial mesenchymal transition pathway |journal=FEBS Lett. |volume=588 |issue=11 |pages=2009–15 |year=2014 |pmid=24786471 |doi=10.1016/j.febslet.2014.04.024 |url=}}
 
* {{cite journal | vauthors = Patel Y, Soni M, Awagulerwitsch A, Kern MJ, Liu S, Shah N, Singh UP, Chen H | title = Overexpression of miR-489 derails mammary hierarchy structure and inhibits HER2/neu-induced tumorigenesis | journal = Oncogene | volume = | issue = | pages = | date = August 2018 | pmid = 30104710 | doi = 10.1038/s41388-018-0439-1 }}
* {{cite journal | vauthors = Patel Y, Lee JS, Chen H | title = Clinicopathological Analysis of miRNA Expression in Breast Cancer Tissues by Using miRNA In Situ Hybridization | journal = Journal of Visualized Experiments : JoVE | volume = | issue = 112 | pages = | date = June 2016 | pmid = 27341462 | pmc = 4922489 | doi = 10.3791/53928 }}
{{refend}}
{{refend}}


{{gene-7-stub}}
{{gene-7-stub}}

Latest revision as of 03:11, 4 September 2018

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Identifiers
Aliases
External IDsGeneCards: [1]
Orthologs
SpeciesHumanMouse
Entrez

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Ensembl

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UniProt

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RefSeq (mRNA)

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RefSeq (protein)

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Location (UCSC)n/an/a
PubMed searchn/an/a
Wikidata
View/Edit Human

MicroRNA 489 is a miRNA that in humans is encoded by the MIR489 gene.[1]

Function

microRNAs (miRNAs) are short (20-24 nt) non-coding RNAs that are involved in post-transcriptional regulation of gene expression in multicellular organisms by affecting both the stability and translation of mRNAs. miRNAs are transcribed by RNA polymerase II as part of capped and polyadenylated primary transcripts (pri-miRNAs) that can be either protein-coding or non-coding. The primary transcript is cleaved by the Drosha ribonuclease III enzyme to produce an approximately 70-nt stem-loop precursor miRNA (pre-miRNA), which is further cleaved by the cytoplasmic Dicer ribonuclease to generate the mature miRNA and antisense miRNA star (miRNA*) products. The mature miRNA is incorporated into a RNA-induced silencing complex (RISC), which recognizes target mRNAs through imperfect base pairing with the miRNA and most commonly results in translational inhibition or destabilization of the target mRNA. The RefSeq represents the predicted microRNA stem-loop. miR-489 acts as tumor suppressor miRNA in breast cancer by inhibiting various oncogenic signaling pathway. It has been demonstrated miR-489 target HER2 and LAPTM4b by directly binding to their 3'UTR. Role of miR-489 has been studied in autochatothus MMTV-Her2 mouse model.[2]

References

  1. ↑ "Entrez Gene: MicroRNA 489".
  2. ↑ Patel Y, Shah N, Lee JS, Markoutsa E, Jie C, Liu S, Botbyl R, Reisman D, Xu P, Chen H (April 2016). "A novel double-negative feedback loop between miR-489 and the HER2-SHP2-MAPK signaling axis regulates breast cancer cell proliferation and tumor growth". Oncotarget. 7 (14): 18295–308. doi:10.18632/oncotarget.7577. PMC 4951289. PMID 26918448.

Further reading

This article incorporates text from the United States National Library of Medicine, which is in the public domain.

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