| identifier |
PRJDB4610 |
| type |
bioproject |
| sameAs |
|
| organism |
Homo sapiens
|
| title |
b-catenin-mediated upregulation of the ASBEL-TCF3 complex is critical for tumorigenicity of colon cancer cells |
| description |
1. The canonical Wnt/b-catenin signaling pathway plays essential roles in the regulation of the self-renewal of stem and progenitor cells, proliferation, and tumorigenesis of cancer cells. To identify novel genes that are the direct targets of b-catenin in colon cancer cells, we performed RNA-seq and ChIP-seq analysis using DLD-1 cells. 2. We found that b-catenin directly upregulates expression of lncRNA ASBEL. We previously identified ASBEL as an antisense transcript of the ANA/BTG3 gene. We further discovered that ASBEL promotes the tumorigenicity of ovarian cancer cells. ASBEL may inhibit ANA/BTG3 protein expression by forming ASBEL-ANA/BTG3 RNA duplexes, which are retained in the nucleus. ASBEL is required for the tumorigenicity of colon tumor cells. We discovered that knockdown of ASBEL increased the expression of ANA/BTG3 protein in colorectal cancer cells. However, ANA/BTG3 protein levels may not be important for the proliferation of colorectal cancer cells. To elucidate the other potential functions of ASBEL in colorectal cancer cells, we analyzed ASBEL-regulated genes by RNA-seq analysis using HCT116 cells. |
| data type |
Epigenomics
|
Transcriptome or Gene Expression
|
| publication |
|
| properties ▽ |
{...}
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| dbXrefs |
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| distribution |
JSONJSON-LD
|
| Download |
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| status |
public |
| visibility |
unrestricted-access |
| dateCreated |
2016-02-29T04:37:53+09:00 |
| dateModified |
2016-10-08T13:07:00+09:00 |
| datePublished |
2016-10-08T13:07:00+09:00 |