Difference between revisions of "BTG3-AS1"

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===Characteristics===
 
===Characteristics===
 
[[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" />.]]
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" />
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ASBEL is transcribed from chromosome 21 (21q21.1), and encodes a conserved, 2-kb ncRNA (termed ASBEL [antisense ncRNA in the ANA/BTG3 (three) locus]). the 5' region of ASBEL is complementary to a portion of the 5' untranslated region (UTR) and the first exon of ANA/BTG3 mRNA <ref name="ref1" />.
  
===Cellular Localization===
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===Function===
21q21.1
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In ovarian carcinoma, ASBEL promotes tumorigenesis through suppressing translation of the sense gene (ANA/BTG3) <ref name="ref1" />. ASBEL 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" /><ref name="ref2" />.  
  
===Function===
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ASBEL also plays a key role in Wnt/β-catenin-mediated tumorigenesis <ref name="ref2" />. ASBEL interacts with and recruits transcription factor 3 (TCF3) to the activating transcription factor 3 (ATF3) locus and represses the expression of ATF3, resulting in proliferation and tumorigenicity of colon tumor cells <ref name="ref2" />
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" />
 
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" />
 
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" />
 
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===
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 ASBEL <ref name="ref2" />.
ATF3 functions as a component in the negative feedback loop that inhibits ASBEL expression.<ref name="ref2" />
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ASBEL represses transcripting of ATF3, and ATF3 functions as a component in the negative feedback loop that inhibits ASBEL expression <ref name="ref2" />.
 
===Disease===
 
===Disease===
Ovarian carcinoma<ref name="ref1" />
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Ovarian carcinoma <ref name="ref1" />
  
colorectal cancer<ref name="ref2" />
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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.<ref name="ref2" />
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ASBEL expression is higher in stage I–III colon cancer than in normal tissues <ref name="ref2" />.
  
 
==Labs working on this lncRNA==
 
==Labs working on this lncRNA==

Revision as of 08:03, 31 July 2017

Annotated Information

Name

BTG3-AS1:BTG3 antisense RNA 1

ASBEL[1]

Characteristics

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

ASBEL is transcribed from chromosome 21 (21q21.1), and encodes a conserved, 2-kb ncRNA (termed ASBEL [antisense ncRNA in the ANA/BTG3 (three) locus]). the 5' region of ASBEL is complementary to a portion of the 5' untranslated region (UTR) and the first exon of ANA/BTG3 mRNA [1].

Function

In ovarian carcinoma, ASBEL promotes tumorigenesis through suppressing translation of the sense gene (ANA/BTG3) [1]. ASBEL 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][2].

ASBEL also plays a key role in Wnt/β-catenin-mediated tumorigenesis [2]. ASBEL interacts with and recruits transcription factor 3 (TCF3) to the activating transcription factor 3 (ATF3) locus and represses the expression of ATF3, resulting in proliferation and tumorigenicity of colon tumor cells [2].

Regulation

β-catenin is found to directly enhance the transcription of ASBEL [2]. ASBEL represses transcripting of ATF3, and ATF3 functions as a component in the negative feedback loop that inhibits ASBEL expression [2].

Disease

Ovarian carcinoma [1]

colorectal cancer [2]

Expression

ASBEL expression is higher in stage I–III colon cancer than in normal tissues [2].

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.[1]
  • Laboratory of Molecular and Genetic Information, Institute of Molecular and Cellular Biosciences, The University of Tokyo, Bunkyo-ku, Tokyo 113-0032, Japan.[2]

References

  1. 1.0 1.1 1.2 1.3 1.4 1.5 1.6 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 for tumorigenicity of ovarian carcinoma. Sci Rep. 2013;3:1305.
  2. 2.0 2.1 2.2 2.3 2.4 2.5 2.6 2.7 Cite error: Invalid <ref> tag; no text was provided for refs named ref2