Difference between revisions of "MIR17HG"
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==Annotated Information== | ==Annotated Information== | ||
| − | === | + | ===Name=== |
| − | MIR17HG | + | Approved Symbol:MIR17HG |
| − | + | ||
| − | miR-17-92a-1 cluster host gene | + | Approved Name:miR-17-92a-1 cluster host gene |
| − | + | ||
| − | C13orf25, MIRHG1 | + | Previous Symbols:C13orf25, MIRHG1 |
| − | + | ||
| − | FLJ14178, MIRH1, MIHG1, NCRNA00048, miR-17-92, LINC00048 | + | Synonyms: FLJ14178, MIRH1, MIHG1, NCRNA00048, miR-17-92, LINC00048 |
| + | |||
| + | RefSeq ID:NR_027349 | ||
| + | |||
| + | Ensembl ID:ENSG00000215417 | ||
| + | |||
| + | LncBook ID: [https://bigd.big.ac.cn/lncbook/transcript?transid=HSALNT0205332 HSALNT0205332] | ||
===Chromosome=== | ===Chromosome=== | ||
13q31.3 | 13q31.3 | ||
| − | + | ||
| − | |||
===OMIM ID=== | ===OMIM ID=== | ||
609415 | 609415 | ||
| − | === | + | ===Disease=== |
| − | + | lymphoma, syndromic developmental defect | |
| − | |||
| − | |||
===Characteristics=== | ===Characteristics=== | ||
Latest revision as of 12:10, 11 August 2019
Contents
Annotated Information
Name
Approved Symbol:MIR17HG
Approved Name:miR-17-92a-1 cluster host gene
Previous Symbols:C13orf25, MIRHG1
Synonyms: FLJ14178, MIRH1, MIHG1, NCRNA00048, miR-17-92, LINC00048
RefSeq ID:NR_027349
Ensembl ID:ENSG00000215417
LncBook ID: HSALNT0205332
Chromosome
13q31.3
OMIM ID
609415
Disease
lymphoma, syndromic developmental defect
Characteristics
miR-17-92 cluster, which comprises seven miRNAs and resides in intron 3 of the C13orf25 gene at 13q31.3 [1].
Cellular Localization
The mir-17–92 polycistron,is located in a region of DNA that is amplified in human B-cell lymphomas.
Function
Gene (MIR17HG), which is involved in the development, progression, and aggressiveness of colorectal cancer [2].
This polycistronic gene, called MIR17HG or Oncomir-1 because of its mainly oncogenic functions (ie, activities that enhance cell proliferation, inhibit apoptosis, and modulate angiogenesis), is related to the homologous MIR106a–363 cluster on chromosome X and the MIR106b–25 cluster on chromosome 7.8,9.[3] [4].
Regulation
Finding of preferential overexpression of the miR-17-92 cluster in lung cancers with small-cell lung cancer histology, a subtype of lung cancer with prominent neuroendocrine feature, warrants study on its regulation and potential involvement from the cell differentiation point of view [1].
Diseases
- colorectal cancer
- lung cancer
Expression
Expression levels of the six MIR17HG cluster members (miR-17, miR-18a, miR-19a, miR-19b-1, miR-20a,and miR-92a-1) were also quantified by RT-qPCR in 34 cases for which RNA was available. In particular, the expression of all six miRs was detected in 23 of 34 cases. miR-19b-1 and miR-92a-1 showed the highest expression level, while miR-18a showed the lowest [2].
Tumours resulting from combined c-myc and mir-17–19b expression consistently invaded visceral organs outside the lymphoid compartment, including liver, lung and occasionally kidney [5].
Sequence
>gi|224994258|ref|NR_027349.1| Homo sapiens miR-17-92a-1 cluster host gene (MIR17HG), transcript variant 2, long non-coding RNA
000081 GGAGGCGGGA GCAGGAGCCC GCGGCCGGCC AGCCGAAGAT GGTGGCGGCT ACTCCTCCTG TCATACACGT GGACCTAACT 000160
000161 GCACCAGTAG CTTTTCTGAG AATACTTGCT GAAAAGGAAG TTTTCTGGAA TGGTATTTGC TAAGTGGAAG CCAGAAGAGG 000240
000241 AGGAAAATGT TTTGCCACGT GGATGTGAAG ATTTCCTCTA AAAGGCAGAC CTGTCTAACT ACAAGCCAGA CTTGGGTTTT 000320
000321 CTCCTGTAGT TTGAAGACAC ACTGACTCCT GACAAAATGC AGCCTGCAAC TTCCTGGAGA ACAACTCAGT GTCACATTAA 000400
000401 AGTTTATTAT GTATTTAATG ATACACTGTT TAATTGACAG TTTTGCATAG TTTGTCTAAC TTTAGAGAAT TAAGAGCCTC 000480
000481 TCAACTGAGC AGTAAAGGTA AGGAGAGCTC AATCTGCACA GAGCCAGTTT TTAGTGTTTG ATGGAAATAA GATCATCATG 000560
000561 CCCACTTGAG ACTTCAGATT ATTCTTTAGC TTAGTGGTTG TATGAGTTAC ATCTTATTAA AGTCGAAATT AATGTAGTTT 000640
000641 TCTGCCTTGA TAACATTTCA TATGTGGTAT TAGTTTTAAA GGGTCATTAG GAAAATGCAC ATATTCCATG AATTTTAAGA 000720
000721 CCCATAGAAA AGTTGAAGAA TGCTTAATTT TCTTATCCAG TAATGTAAAC ACAGAGACAG AACATTGAGA TGTGCCTAGT 000800
000801 TCTGTATTTA CAGTTTGGTC TGGCTGTTTG AGTTCTAGCG CATTTAATGT TAATAAATAA AATACTGCAT TTTAAAGCTG 000880
000881 TTAAGAAATT GTCCAGAACG AGAATATTGA AATAAAAACT TCAAGGT
Labs working on this lncRNA
Krannert Institute of Cardiology and Division of Cardiology, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana 46202, USA .[2]
Computational Medicine Center, Thomas Jefferson University, Philadelphia, PA 19107, USA. [3].
Division of Cellular and Developmental Biology, MCB Department, University of California at Berkeley, Berkeley, CA 94705, USA. [4].
Cold Spring Harbor Laboratory, Watson School of Biological Sciences, 1 Bungtown Road, Cold Spring Harbor, New York 11724, USA. [5].
Division of Molecular Oncology, Aichi Cancer Center Research Institute, Japan.[1].
References
- ↑ 1.0 1.1 1.2 Yoji Hayashita, Hirotaka Osada, Yoshio Tatematsu, Hideki Yamada, Kiyoshi Yanagisawa, Shuta Tomida, Yasushi Yatabe, Katsunobu Kawahara, Yoshitaka Sekido, Takashi Takahashi (2005) A Polycistronic MicroRNA Cluster, miR-17-92, Is Overexpressed in Human Lung Cancers and Enhances Cell Proliferation.Cancer Research CAN-05-2352.
- ↑ 2.0 2.1 2.2 Han P, Li W, Lin CH, Yang J, Shang C, Nurnberg ST, Jin KK, Xu W, Lin CY, Lin CJ, Xiong Y, Chien HC, Zhou B, Ashley E, Bernstein D, Chen PS, Chen HS, Quertermous T, Chang CP.(2014) A long non-coding RNA protects the heart from pathologicalhypertrophy. Nature 514(7520):102-6 .
- ↑ 3.0 3.1 Mogilyansky E, Rigoutsos I. (2013)The miR-17/92 cluster: a comprehensive update on its genomics, genetics, functions and increasingly important and numerous roles in health and disease. Cell Death Differ. 20(12):1603–1614 .
- ↑ 4.0 4.1 Olive V, Li Q, He L. Mir-17-92: a polycistronic oncomir with pleiotropic functions. Immunol Rev. 2013;253(1):158–166.
- ↑ 5.0 5.1 Lin He1, J. Michael Thomson, Michael T. Hemann1, Eva Hernando-Monge4, David Mu1,Summer Goodson2, Scott Powers1, Carlos Cordon-Cardo4, Scott W. Lowe1, Gregory J. Hannon1, and Scott M. Hammond.(2005)A microRNA polycistron as a potential human oncogene.Nature 435(7043): 828–833.
