Difference between revisions of "BTG3-AS1"
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==Annotated Information== | ==Annotated Information== | ||
| − | === | + | ===Name=== |
| − | BTG3-AS1 | + | BTG3-AS1:BTG3 antisense RNA 1 |
| − | + | ||
| − | BTG3 antisense RNA 1 | + | ASBEL<ref name="ref1" /> |
| − | = | + | |
| − | + | ===Characteristics=== | |
| − | === | + | [[File:ASBEL-1.JPG|right|thumb|400px|'''ASBEL is transcribed from the DNA strand opposite to ANA/BTG3'''<ref name="ref1" />.]] |
| − | ASBEL | + | 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" /> |
| − | === | + | |
| + | ===Cellular Localization=== | ||
21q21.1 | 21q21.1 | ||
| − | === | + | |
| − | + | ===Function=== | |
| − | == | + | 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=== |
| + | 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" /> | ||
| + | ATF3 functions as a component in the negative feedback loop that inhibits ASBEL expression.<ref name="ref2" /> | ||
===Disease=== | ===Disease=== | ||
| − | Ovarian carcinoma | + | Ovarian carcinoma<ref name="ref1" /> |
| + | |||
| + | colorectal cancer<ref name="ref2" /> | ||
| + | ===Expression=== | ||
| + | ASBEL expression is higher in stage I–III colon cancer than in normal tissues. | ||
| + | |||
| + | ==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. | ||
| + | ==References== | ||
| + | <references> | ||
| + | <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 for | ||
| + | tumorigenicity of ovarian carcinoma. Sci Rep. 2013;3:1305. | ||
| + | </ref> | ||
| + | <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. | ||
| + | </references> | ||
| + | |||
| + | [[Category: Antisense]] | ||
Revision as of 03:23, 27 July 2017
Contents
Annotated Information
Name
BTG3-AS1:BTG3 antisense RNA 1
ASBEL[1]
Characteristics
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.[1]
Cellular Localization
21q21.1
Function
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.[1] 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.[1] 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 [2] 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[2]
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).[2] 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.
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.
References
- ↑ 1.0 1.1 1.2 1.3 1.4 1.5 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 Cite error: Invalid
<ref>tag; no text was provided for refs namedref2
