Difference between revisions of "DEC1"
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− | ''DEC1'', | + | ''DEC1'', a candidate tumor suppressor in 9q32 |
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==Annotated Information== | ==Annotated Information== | ||
===Name=== | ===Name=== | ||
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===Disease=== | ===Disease=== | ||
− | * | + | *esophageal squamous cell carcinoma <ref name="ref1" /><ref name="ref2" /> |
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===Expression=== | ===Expression=== | ||
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==Labs working on this lncRNA== | ==Labs working on this lncRNA== | ||
− | *Laboratory of Molecular | + | *Laboratory of Molecular Medicine, Human Genome Center, Institute of Medical Science, University of Tokyo, Tokyo, Japan. |
− | *Laboratory of Molecular | + | *Laboratory of Molecular Medicine, The Institute of Medical Science, The University of Tokyo, Japan. |
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==References== | ==References== | ||
<references> | <references> | ||
− | <ref name="ref1"> </ref>(1) | + | <ref name="ref1"> Nishiwaki T, Daigo Y, Kawasoe T, Nakamura Y. Isolation and mutational analysis of a novel human cDNA, DEC1 (deleted in esophageal cancer 1), derived from the tumor suppressor locus in 9q32. Genes Chromosomes Cancer. 2000 Feb;27(2):169-76.</ref>(1) |
− | <ref name="ref2"> </ref>(2) | + | <ref name="ref2">Miura K, Suzuki K, Tokino T, Isomura M, Inazawa J, Matsuno S, Nakamura Y. Detailed deletion mapping in squamous cell carcinomas of the esophagus narrows a region containing a putative tumor suppressor gene to about 200 kilobases on distal chromosome 9q. Cancer Res. 1996 Apr 1;56(7):1629-34. </ref>(2) |
</references> | </references> | ||
Revision as of 09:17, 12 June 2019
DEC1, a candidate tumor suppressor in 9q32
Contents
Annotated Information
Name
DEC1': deleted in esophageal cancer 1
Characteristics
BTB3-AS1 is a member of the TOB/BTG family of antiproliferative genes that regulates cell cycle progression in a variety of cell types [1]
BTB3-AS1 is an antisense transcript of ANA/BTG3. it is a highly conserved gene encoded by the DNA strand opposite the ANA/BTG3 gene.
Function
In ovarian carcinoma, BTB3-AS1 promotes tumorigenesis through suppressing translation of the sense gene (ANA/BTG3) [2]. BTB3-AS1 forms duplexes with ANA/BTG3 mRNA in the nucleus and suppresses its cytoplasmic transportation, leading to negative regulation of ANA/BTG3 at protein level without changing of its mRNA level [2]. BTB3-AS1 also plays a key role in Wnt/β-catenin-mediated tumorigenesis [3]. BTB3-AS1 interacts with and recruits transcription factor 3 (TCF3) for activating transcription factor 3 (ATF3) locus and represses the expression of ATF3, resulting in proliferation and tumorigenicity of colon tumor cells [3].
Regulation
β-catenin is found to directly enhance the transcription of BTB3-AS1 [3].
Disease
Expression
BTB3-AS1 is highly expressed in stage I–III colon cancer than in normal tissues [3].
Labs working on this lncRNA
- Laboratory of Molecular Medicine, Human Genome Center, Institute of Medical Science, University of Tokyo, Tokyo, Japan.
- Laboratory of Molecular Medicine, The Institute of Medical Science, The University of Tokyo, Japan.
References
- ↑ Cite error: Invalid
<ref>
tag; no text was provided for refs namedref3
- ↑ 2.0 2.1 2.2 2.3 Nishiwaki T, Daigo Y, Kawasoe T, Nakamura Y. Isolation and mutational analysis of a novel human cDNA, DEC1 (deleted in esophageal cancer 1), derived from the tumor suppressor locus in 9q32. Genes Chromosomes Cancer. 2000 Feb;27(2):169-76.
- ↑ 3.0 3.1 3.2 3.3 3.4 Miura K, Suzuki K, Tokino T, Isomura M, Inazawa J, Matsuno S, Nakamura Y. Detailed deletion mapping in squamous cell carcinomas of the esophagus narrows a region containing a putative tumor suppressor gene to about 200 kilobases on distal chromosome 9q. Cancer Res. 1996 Apr 1;56(7):1629-34.
Sequence
>PREDICTED: Homo sapiens deleted in esophageal cancer 1 (DEC1), transcript variant X1
000081 GGTTTTTACT GATGCCCTGC ACAGAGAGAG GTCTGTAAAG TGGCAAGCAG GAGTCTGCTA CAATGGAGGA AAGGATTTTG 000160
000161 CTGTATCTCT TGCCAGGCCC AAGGCTGCAG AGGGAATTGG TAATATACTT CATTTAATAA TAGTGTTTTA AGGGACATTA 000240
000241 TCATTTCATC CTATGTGGTA GATGTGATCA TCTTCATCTC ACAGATGAAA AGAGACAAAC CTGGGATTCA GAGGTACTTG 000320
000321 CCTATGAGTT TCTTACAGAT TTCCTCTTAC AATCCAGAAC TGCTGATTCC TGGGTCAGTG TCCTTTCCAA TATGGCATCT 000400
000401 TAGGCATGGC AATAAGTGAG ATCTAAAAGC TAGTTATTTG ATGCTTGGAC AAAGGCTTAG GGCATGGGCT TTGACCTAAT 000480
000481 GAATCAGTAG ATTCTAGTCT AATATTTTAA AGGATTTGAA ATGATTCCAG TTTATAAGCC CCTTTAACTG TCTTCTAAGA 000560
000561 TGTGGCTAAA CATTCCAACC TTCCTTAGCT CAAAAGTGGA CAAAACAAGA GATTACACAT GTTGATACTT TGGGAGTCAT 000640
000641 AGAAAATTCA CATATACATA GGCAGAGTGG TTCTGTAATT AACCAAATCT TTAGAGGTCC AAGGTTAACA GTATTGACCA 000720
000721 TTCATAATTA GCCATAAACT CAGACATTTT AAAAGCCTCA TGAAAATAGA AGTATAGTTT TCAAATGTTA CAGACCCCAA 000800
000801 ACACCAGTGT TTTATTGCCT ACAGCAAGCA TAGCTCACAG ATCATCAC