Difference between revisions of "MIR17HG"
(Created page with "==Annotated Information== ===Approved Symbol=== MIR17HG ===Approved Name=== miR-17-92a-1 cluster host gene ===Previous Symbols=== C13orf25, MIRHG1 ===Synonyms=== FLJ14178, MIR...") |
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===pubmed IDs=== | ===pubmed IDs=== | ||
15126345, 15944707, 16266980, 17210683, 23551855 | 15126345, 15944707, 16266980, 17210683, 23551855 | ||
| + | |||
| + | ===Characteristics=== | ||
| + | miR-17-92 cluster, which comprises seven miRNAs and resides in intron 3 of the C13orf25 gene at 13q31.3 <ref name="ref5" />. | ||
| + | |||
| + | ===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 <ref name="ref1" />. | ||
| + | |||
| + | 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.<ref name="ref2" /> <ref name="ref3" />. | ||
| + | |||
| + | ===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 <ref name="ref5" />. | ||
| + | |||
| + | ===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 <ref name="ref1" />. | ||
| + | |||
| + | 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 <ref name="ref4" />. | ||
| + | |||
===Sequence=== | ===Sequence=== | ||
>gi|224994258|ref|NR_027349.1| Homo sapiens miR-17-92a-1 cluster host gene (MIR17HG), transcript variant 2, long non-coding RNA | >gi|224994258|ref|NR_027349.1| Homo sapiens miR-17-92a-1 cluster host gene (MIR17HG), transcript variant 2, long non-coding RNA | ||
<dnaseq>GAAGCTCTCCTCGCGGGGCGGGCCGGCCGGCCGCACCCCCGGCCTGGGGCCTCCGGTCGTAGTAAAGCGCAGGCGGGCGGGGAGGCGGGAGCAGGAGCCCGCGGCCGGCCAGCCGAAGATGGTGGCGGCTACTCCTCCTGTCATACACGTGGACCTAACTGCACCAGTAGCTTTTCTGAGAATACTTGCTGAAAAGGAAGTTTTCTGGAATGGTATTTGCTAAGTGGAAGCCAGAAGAGGAGGAAAATGTTTTGCCACGTGGATGTGAAGATTTCCTCTAAAAGGCAGACCTGTCTAACTACAAGCCAGACTTGGGTTTTCTCCTGTAGTTTGAAGACACACTGACTCCTGACAAAATGCAGCCTGCAACTTCCTGGAGAACAACTCAGTGTCACATTAAAGTTTATTATGTATTTAATGATACACTGTTTAATTGACAGTTTTGCATAGTTTGTCTAACTTTAGAGAATTAAGAGCCTCTCAACTGAGCAGTAAAGGTAAGGAGAGCTCAATCTGCACAGAGCCAGTTTTTAGTGTTTGATGGAAATAAGATCATCATGCCCACTTGAGACTTCAGATTATTCTTTAGCTTAGTGGTTGTATGAGTTACATCTTATTAAAGTCGAAATTAATGTAGTTTTCTGCCTTGATAACATTTCATATGTGGTATTAGTTTTAAAGGGTCATTAGGAAAATGCACATATTCCATGAATTTTAAGACCCATAGAAAAGTTGAAGAATGCTTAATTTTCTTATCCAGTAATGTAAACACAGAGACAGAACATTGAGATGTGCCTAGTTCTGTATTTACAGTTTGGTCTGGCTGTTTGAGTTCTAGCGCATTTAATGTTAATAAATAAAATACTGCATTTTAAAGCTGTTAAGAAATTGTCCAGAACGAGAATATTGAAATAAAAACTTCAAGGT</dnaseq> | <dnaseq>GAAGCTCTCCTCGCGGGGCGGGCCGGCCGGCCGCACCCCCGGCCTGGGGCCTCCGGTCGTAGTAAAGCGCAGGCGGGCGGGGAGGCGGGAGCAGGAGCCCGCGGCCGGCCAGCCGAAGATGGTGGCGGCTACTCCTCCTGTCATACACGTGGACCTAACTGCACCAGTAGCTTTTCTGAGAATACTTGCTGAAAAGGAAGTTTTCTGGAATGGTATTTGCTAAGTGGAAGCCAGAAGAGGAGGAAAATGTTTTGCCACGTGGATGTGAAGATTTCCTCTAAAAGGCAGACCTGTCTAACTACAAGCCAGACTTGGGTTTTCTCCTGTAGTTTGAAGACACACTGACTCCTGACAAAATGCAGCCTGCAACTTCCTGGAGAACAACTCAGTGTCACATTAAAGTTTATTATGTATTTAATGATACACTGTTTAATTGACAGTTTTGCATAGTTTGTCTAACTTTAGAGAATTAAGAGCCTCTCAACTGAGCAGTAAAGGTAAGGAGAGCTCAATCTGCACAGAGCCAGTTTTTAGTGTTTGATGGAAATAAGATCATCATGCCCACTTGAGACTTCAGATTATTCTTTAGCTTAGTGGTTGTATGAGTTACATCTTATTAAAGTCGAAATTAATGTAGTTTTCTGCCTTGATAACATTTCATATGTGGTATTAGTTTTAAAGGGTCATTAGGAAAATGCACATATTCCATGAATTTTAAGACCCATAGAAAAGTTGAAGAATGCTTAATTTTCTTATCCAGTAATGTAAACACAGAGACAGAACATTGAGATGTGCCTAGTTCTGTATTTACAGTTTGGTCTGGCTGTTTGAGTTCTAGCGCATTTAATGTTAATAAATAAAATACTGCATTTTAAAGCTGTTAAGAAATTGTCCAGAACGAGAATATTGAAATAAAAACTTCAAGGT</dnaseq> | ||
| + | |||
| + | ==Labs working on this lncRNA== | ||
| + | * Division of Cardiovascular Medicine, Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA 94305 <ref name="ref1" />. | ||
| + | * Cold Spring Harbor Laboratory, Watson School of Biological Sciences, 1 Bungtown Road, Cold Spring Harbor, New York 11724, USA <ref name="ref1" />. | ||
| + | |||
| + | ==References== | ||
| + | <references> | ||
| + | <ref name="ref1"> 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 .</ref>(1) | ||
| + | <ref name="ref2"> 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 .</ref>(2) | ||
| + | <ref name="ref3"> Olive V, Li Q, He L. Mir-17-92: a polycistronic oncomir with pleiotropic functions. Immunol Rev. 2013;253(1):158–166.</ref>(3) | ||
| + | <ref name="ref4"> 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.</ref>(4) | ||
| + | <ref name="ref5"> 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.</ref>(5) | ||
| + | </references> | ||
Revision as of 02:42, 29 June 2016
Annotated Information
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
Chromosome
13q31.3
RefSeq ID
NR_027349
OMIM ID
609415
Ensembl ID
ENSG00000215417
pubmed IDs
15126345, 15944707, 16266980, 17210683, 23551855
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
000001 GAAGCTCTCC TCGCGGGGCG GGCCGGCCGG CCGCACCCCC GGCCTGGGGC CTCCGGTCGT AGTAAAGCGC AGGCGGGCGG 000080
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
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
- Division of Cardiovascular Medicine, Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA 94305 [2].
- Cold Spring Harbor Laboratory, Watson School of Biological Sciences, 1 Bungtown Road, Cold Spring Harbor, New York 11724, USA [2].
References
- ↑ 1.0 1.1 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 2.3 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 .
- ↑ 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 .
- ↑ Olive V, Li Q, He L. Mir-17-92: a polycistronic oncomir with pleiotropic functions. Immunol Rev. 2013;253(1):158–166.
- ↑ 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.
