Difference between revisions of "BTG3-AS1"

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''BTB3-AS1'', an antinsense transcript required for tumorogenicity of ovarian and colorectal cancer cells
 +
 
==Annotated Information==
 
==Annotated Information==
 
===Name===
 
===Name===
−
BTG3-AS1:BTG3 antisense RNA 1
+
''BTB3-AS1'': BTG3 antisense RNA 1
−
 
+
ASBEL <ref name="ref1" />
−
ASBEL<ref name="ref1" />
 
  
 
===Characteristics===
 
===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 <ref name="ref3" />
 
[[File:ASBEL-1.JPG|right|thumb|400px|'''ASBEL is transcribed from the DNA strand opposite to ANA/BTG3'''<ref name="ref1" />.]]
 
[[File:ASBEL-1.JPG|right|thumb|400px|'''ASBEL is transcribed from the DNA strand opposite to ANA/BTG3'''<ref name="ref1" />.]]
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ASBEL, an antisense transcript of ANA/BTG3, is a highly conserved gene encoded by the DNA strand opposite the ANA/BTG3 gene. This gene encodes a conserved, 2-kb ncRNA (termed ASBEL [antisense ncRNA in the ANA/BTG3 (three) locus]), the 5' region of which is complementary to a portion of the 5' untranslated region (UTR) and the first exon of ANA/BTG3 mRNA.<ref name="ref1" />
+
''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.
−
 
 
−
===Cellular Localization===
 
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21q21.1
 
  
 
===Function===
 
===Function===
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Knockdown of ASBEL causes a significant reduction in the growth of the clear cell adenocarcinoma (CCC cell) lines JHOC5, JHOC9, and OVISE and the serous adenocarcinoma cell lines OV1063 and 2008 cells. In addition, knockdown of ASBEL induced apoptosis of JHOC5 cells.<ref name="ref1" />
+
In ovarian carcinoma, ''BTB3-AS1'' promotes tumorigenesis through suppressing translation of the sense gene (ANA/BTG3) <ref name="ref1" />. ''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 <ref name="ref1" />.
−
Knockdown of ASBEL using siRNA (siASBEL) results in an increase in the levels of ANA/BTG3 protein, but not mRNA. And Knockdown of ASBEL using shASBEL also does not affect the levels of ANA/BTG3 mRNA. By contrast, overexpression of ASBEL decreases the levels of ANA/BTG protein, but not mRNA, compared to that of antisense ASBEL. In addition, ASBEL forms duplexes with ANA/BTG3 mRNA in the nucleus and suppresses its cytoplasmic transportation.<ref name="ref1" />
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''BTB3-AS1'' also plays a key role in Wnt/β-catenin-mediated tumorigenesis <ref name="ref2" />. ''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 <ref name="ref2" />. 
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Knockdown of ASBEL by siRNA (siASBEL) causes a significant reduction in the growth of DLD-1, HCT116, and Caco2 cells but not of normal keratinocyte HaCaT cells in vitro and leads to a marked increase in apoptotic cell death of HCT116 cells but not of HaCaT cells. Moreover, knockdown of ASBEL reduces the invasiveness of DLD-1 and HCT116 cells <ref name="ref2" />
 
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ASBEL forms complexes with ANA/BTG3 mRNA in the nucleus and suppresses its cytoplasmic transportation, thereby suppressing the levels of ANA/BTG3 protein. And ASBEL–TCF3 complex–mediated down-regulation of activating transcription factor 3 (ATF3) is required for the tumorigenicity of colon cancer cells<ref name="ref2" />
 
  
 
===Regulation===
 
===Regulation===
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β-catenin directly enhances the transcription of the lncRNA ASBEL [antisense ncRNA in the Abundant in neuroepithelium area (ANA)/B-cell translocation gene 3 (BTG3) locus] and transcription factor 3 (TCF3).<ref name="ref2" />
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β-catenin is found to directly enhance the transcription of ''BTB3-AS1'' <ref name="ref2" />.
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ATF3 functions as a component in the negative feedback loop that inhibits ASBEL expression.<ref name="ref2" />
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===Disease===
 
===Disease===
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Ovarian carcinoma<ref name="ref1" />
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*Colorectal cancer <ref name="ref2" />
 +
*Ovarian carcinoma <ref name="ref1" />
  
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colorectal cancer<ref name="ref2" />
 
 
===Expression===
 
===Expression===
−
ASBEL expression is higher in stage I–III colon cancer than in normal tissues.
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''BTB3-AS1'' is highly expressed in stage I–III colon cancer than in normal tissues <ref name="ref2" />.
  
 
==Labs working on this lncRNA==
 
==Labs working on this lncRNA==
 
*Laboratory of Molecular and Genetic Information, Institute of Molecular and Cellular Biosciences, The University of Tokyo, 1-1-1 Yayoi, Bunkyo-ku, Tokyo 113-0032, Japan.
 
*Laboratory of Molecular and Genetic Information, Institute of Molecular and Cellular Biosciences, The University of Tokyo, 1-1-1 Yayoi, Bunkyo-ku, Tokyo 113-0032, Japan.
 
*Laboratory of Molecular and Genetic Information, Institute of Molecular and Cellular Biosciences, The University of Tokyo, Bunkyo-ku, Tokyo 113-0032, Japan.
 
*Laboratory of Molecular and Genetic Information, Institute of Molecular and Cellular Biosciences, The University of Tokyo, Bunkyo-ku, Tokyo 113-0032, Japan.
 +
*Division of Oncology, Department of Cancer Biology, Institute of Medical Science, The University of Tokyo, 461 Shirokanedai, Tokyo, 108-8639, Japan.
 +
 +
 
==References==
 
==References==
 
<references>
 
<references>
−
<ref name="ref1">
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<ref name="ref1">Yanagida S, Taniue K, Sugimasa H, Nasu E, Takeda Y, Kobayashi M, Yamamoto T,Okamoto A, Akiyama T. ASBEL, an ANA/BTG3 antisense transcript required fortumorigenicity of ovarian carcinoma. Sci Rep. 2013;3:1305.
−
Yanagida S, Taniue K, Sugimasa H, Nasu E, Takeda Y, Kobayashi M, Yamamoto T,
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</ref>(1)
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Okamoto A, Akiyama T. ASBEL, an ANA/BTG3 antisense transcript required for
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<ref name="ref2">Taniue K, Kurimoto A, Takeda Y, Nagashima T, Okada-Hatakeyama M, Katou Y, Shirahige K, Akiyama T. ASBEL-TCF3 complex is required for the tumorigenicity of colorectal cancer cells. Proc Natl Acad Sci U S A. 2016 Oct 21.
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tumorigenicity of ovarian carcinoma. Sci Rep. 2013;3:1305.
+
</ref>(2)
−
</ref>
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<ref name="ref3">Winkler, G. S. The mammalian anti-proliferative BTG/Tob protein family. J. Cell.
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<ref name="ref2">
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Phys. 222, 66–72 (2010).
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Taniue K, Kurimoto A, Takeda Y, Nagashima T, Okada-Hatakeyama M, Katou Y,
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</ref>(3)
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Shirahige K, Akiyama T. ASBEL-TCF3 complex is required for the tumorigenicity of  
 
−
colorectal cancer cells. Proc Natl Acad Sci U S A. 2016 Oct 21.
 
 
</references>
 
</references>
  
−
[[Category: Antisense]]
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===Sequence===
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>gi|110806272|ref|NR_149073.1|Homo sapiens BTG3 antisense RNA 1 (BTG3-AS1), long non-coding RNA
 +
<dnaseq>ATCGCACGGTGACGTCATCCTGGGACCTCGTCACCGCGGCGGCTGCTCCTCAAGTTCTACTTTGTTCCAC
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AAGGCTCCTCTGCTCACGGCTGCGTGGATAAAACCCAAAGGGAATCCAGAATCAAGCTCGGCCTCGCAGG
 +
AGTTTATAACTTTTGTACTTTTCCCTCCCTTGTAACGAAAAGCTAATCGCAAACGTTTCTAGGAACACAT
 +
TTTTCTCCTGATAGACGTTCCCAAGGTGGAGGGCGCGAGAAGACTGGCCCGTGGGGTGAGGAGCCCCGGC
 +
CCGACCTCAGCGGCGCCACAAAGCCATGAAGAGGGGAAATAATTTTCCAAGGGGCTAAGAGTTGGACTTT
 +
CTGAAGCCATCGAAACCTGCTGCTAGGCTCTCCCGCTGGGGTTTTGAGAGAGGTAGGTGAGGAGGGATCA
 +
AACATCTCCACCCGCTCTTGAAAGAACCGCCTTGAGCTGCGCCCAACTTCTGCAATCCCGGTTTTCCCCA
 +
AGTTCAAGGGGAAGGGCCCTGGCGCCCAATGCCCAGCCTCCCCGACAACATCCTCGCCAGGGTGCGCCTG
 +
CCCCGCGGGTCCGCTGTCCCCGGCGGGCGGCCCTGGGTTCGAGGACCCGGCTTCCCGGAGGCGCGACTCT
 +
CCAGCAAACAAGCGGAGCTCCAGAAAAAACACCGACGCGAAGGGGGTGGACAGAGGGTGGGAAGCCGCGG
 +
GGTTGTCGCCCACCCGGAGGCGGAATGTAACGCGCTGTGGGAAACGTGGCAGGAGCCCTGAGGCGGCGTC
 +
TTTTTCCTCAGGCGCCCGCCGAGGGTCCCGCGGAAAGCCTCGCGGGCCGCCCTCGCGGCCCGCAGCCCCG
 +
CTCTGGCGCCGAGCCGGAGCCCATGCAACCTGGTTCCATCCCCTGCCCCTCCCCTGTCCCCGGTGCGCCG
 +
CCCGCCAGCGAGCCTTCGACGTGGCCGCAGGGGCGACGGGACCACCCTCCCCCGATACCCACAGCCCCGC
 +
CATGTCTGCCTTTCCCCGGCCCGGTCTCCTCACCGCCGCTGCCGCCGCCGCTCTTCGGCCGGAGATTCGG
 +
CGGCCCAGACCGTGTCCTGGCCGGGAACTGAGGGCTCCGCCTCAACGGGCCCGCGCTGGGCAACAGGGAG
 +
CGCAGCGAGCCTCGTCCGGCGCGTGCGGCTCCCGCGTCGTCGGGCGGCCAAGCGCGCGTTGAGAGGACTG
 +
GCGGGCGGACGAGCGCGCACACGAGTGAGCGCAGCCCCAAAGCGGCGCGCAGGGGGCTCGCGGCCCGGAA
 +
GAGGGGAGGGGCGATGACCCGGGAAAGGGTTGGCGCGCGCGGGATCGGCTCGCGCGCCTGAGGGGCGGTG
 +
CCGGGGGCGGGGCTTCGCCGCGAGGCCACCCCCGAGCCCCGGGCCTAGCCGCACGGGAGGCGACACACCC
 +
TCGCCCTACCCTGAGCCTGGCGCAGACCCTCGACCGCGACGGCGCGGTCCGCAGAACCGCGGGCTTCCCT
 +
CCCCGGCAAAAAGCGGCGCTGAAGGCCTGTGGGACCCCCGCCCGGCCGCCCTACGTGCGTCAGCGCCTTC
 +
GGGGGTCGCGCGGGCTTGGTCCTTTCGGCTGTCTCGGCCTTTTTGTTTCCCCCTCAGGTCTCTCCACGCT
 +
GCACTTGACACCCTCAGGGCGGAATGGCGAGTTCTAGACCCAGCTCTCTAGACCCGGGGCTTCATGGGGG
 +
ACACGGACTCGACGGGAAGGGGAACTTGGCATTTATGGACAGATCCTCATCCTTCTTGCTGTAGTCAATT
 +
ACACGCACGTTAACCGTGCAGCCGCCCTGCTGTATTTTAGGCGGTTGTTGGCACTCCTAGTTGGGCCCTT
 +
CCCTGGCCCCTCACAGCAGGGCCTGCCTCCTGTGGACGCTTGTGTGCTGCCCTGGCACCGGCCACTGTGT
 +
TTTGCATAAAGGAGAGGCTCCAAAGATGTTGGCCAAAGGAATGAAGCCTTGAGAGTCCAGGCTTTCTATT
 +
TCTGAGACACTCTACTCAAGGACTTCCCAGATGCAAAGCTTCATCTTTGAGCAAATACAAATATGGAGAG
 +
GGAACATTAACTTTCTGAAGAAAAGAAGGAACATCTTTTCAACCTTTTATATTGAGTTAACACCATGGTC
 +
TTAGTTTTGTGAAAGCACTTTAATACATCCAACTAGCGGGAGGAATACAAGATATTCCTACCTTTTTATT
 +
ATTATTATTAAAAGAGGGCTAAACCATGTTGTAAACTACTTAAGAACTGAATGTTCAAGTTGTACAGTAT
 +
ATTGGCCAGATTCCTTACTGCCCACTAGGCTTGGGAGCATGTTTTCAGCTCAGTTTTATGAATGTTTTAA
 +
ATTTGTATTACTGATCTTTGTTATAGCCAATTAGCAATTCAAAATGGTAATTTTTTTAGCAGTAATAAAT
 +
ATACCATCCCCCAAACAGTACAATAAACTTTATTTGTAAAAAAAAAAAAAAAAAA</dnaseq>

Latest revision as of 05:04, 14 November 2018

BTB3-AS1, an antinsense transcript required for tumorogenicity of ovarian and colorectal cancer cells

Annotated Information

Name

BTB3-AS1: BTG3 antisense RNA 1 ASBEL [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 [2]

ASBEL is transcribed from the DNA strand opposite to ANA/BTG3[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) [1]. 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 [1]. 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

  • Colorectal cancer [3]
  • Ovarian carcinoma [1]

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 and Genetic Information, Institute of Molecular and Cellular Biosciences, The University of Tokyo, 1-1-1 Yayoi, Bunkyo-ku, Tokyo 113-0032, Japan.
  • Laboratory of Molecular and Genetic Information, Institute of Molecular and Cellular Biosciences, The University of Tokyo, Bunkyo-ku, Tokyo 113-0032, Japan.
  • Division of Oncology, Department of Cancer Biology, Institute of Medical Science, The University of Tokyo, 461 Shirokanedai, Tokyo, 108-8639, Japan.


References

  1. ↑ 1.0 1.1 1.2 1.3 1.4 Yanagida S, Taniue K, Sugimasa H, Nasu E, Takeda Y, Kobayashi M, Yamamoto T,Okamoto A, Akiyama T. ASBEL, an ANA/BTG3 antisense transcript required fortumorigenicity of ovarian carcinoma. Sci Rep. 2013;3:1305.
  2. ↑ Winkler, G. S. The mammalian anti-proliferative BTG/Tob protein family. J. Cell. Phys. 222, 66–72 (2010).
  3. ↑ 3.0 3.1 3.2 3.3 3.4 Taniue K, Kurimoto A, Takeda Y, Nagashima T, Okada-Hatakeyama M, Katou Y, Shirahige K, Akiyama T. ASBEL-TCF3 complex is required for the tumorigenicity of colorectal cancer cells. Proc Natl Acad Sci U S A. 2016 Oct 21.

Sequence

>gi|110806272|ref|NR_149073.1|Homo sapiens BTG3 antisense RNA 1 (BTG3-AS1), long non-coding RNA

000001 ATCGCACGGT GACGTCATCC TGGGACCTCG TCACCGCGGC GGCTGCTCCT CAAGTTCTAC TTTGTTCCAC AAGGCTCCTC 000080
000081 TGCTCACGGC TGCGTGGATA AAACCCAAAG GGAATCCAGA ATCAAGCTCG GCCTCGCAGG AGTTTATAAC TTTTGTACTT 000160
000161 TTCCCTCCCT TGTAACGAAA AGCTAATCGC AAACGTTTCT AGGAACACAT TTTTCTCCTG ATAGACGTTC CCAAGGTGGA 000240
000241 GGGCGCGAGA AGACTGGCCC GTGGGGTGAG GAGCCCCGGC CCGACCTCAG CGGCGCCACA AAGCCATGAA GAGGGGAAAT 000320
000321 AATTTTCCAA GGGGCTAAGA GTTGGACTTT CTGAAGCCAT CGAAACCTGC TGCTAGGCTC TCCCGCTGGG GTTTTGAGAG 000400
000401 AGGTAGGTGA GGAGGGATCA AACATCTCCA CCCGCTCTTG AAAGAACCGC CTTGAGCTGC GCCCAACTTC TGCAATCCCG 000480
000481 GTTTTCCCCA AGTTCAAGGG GAAGGGCCCT GGCGCCCAAT GCCCAGCCTC CCCGACAACA TCCTCGCCAG GGTGCGCCTG 000560
000561 CCCCGCGGGT CCGCTGTCCC CGGCGGGCGG CCCTGGGTTC GAGGACCCGG CTTCCCGGAG GCGCGACTCT CCAGCAAACA 000640
000641 AGCGGAGCTC CAGAAAAAAC ACCGACGCGA AGGGGGTGGA CAGAGGGTGG GAAGCCGCGG GGTTGTCGCC CACCCGGAGG 000720
000721 CGGAATGTAA CGCGCTGTGG GAAACGTGGC AGGAGCCCTG AGGCGGCGTC TTTTTCCTCA GGCGCCCGCC GAGGGTCCCG 000800
000801 CGGAAAGCCT CGCGGGCCGC CCTCGCGGCC CGCAGCCCCG CTCTGGCGCC GAGCCGGAGC CCATGCAACC TGGTTCCATC 000880
000881 CCCTGCCCCT CCCCTGTCCC CGGTGCGCCG CCCGCCAGCG AGCCTTCGAC GTGGCCGCAG GGGCGACGGG ACCACCCTCC 000960
000961 CCCGATACCC ACAGCCCCGC CATGTCTGCC TTTCCCCGGC CCGGTCTCCT CACCGCCGCT GCCGCCGCCG CTCTTCGGCC 001040
001041 GGAGATTCGG CGGCCCAGAC CGTGTCCTGG CCGGGAACTG AGGGCTCCGC CTCAACGGGC CCGCGCTGGG CAACAGGGAG 001120
001121 CGCAGCGAGC CTCGTCCGGC GCGTGCGGCT CCCGCGTCGT CGGGCGGCCA AGCGCGCGTT GAGAGGACTG GCGGGCGGAC 001200
001201 GAGCGCGCAC ACGAGTGAGC GCAGCCCCAA AGCGGCGCGC AGGGGGCTCG CGGCCCGGAA GAGGGGAGGG GCGATGACCC 001280
001281 GGGAAAGGGT TGGCGCGCGC GGGATC