BTG3-AS1
Contents
Annotated Information
Name
BTG3-AS1:BTG3 antisense RNA 1
ASBEL[1]
Characteristics
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
- ↑ 1.0 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.
- ↑ 2.0 2.1 2.2 2.3 2.4 2.5 2.6 2.7 Cite error: Invalid
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