Project Detail : PRJDB4610

AccessionPRJDB4610
Project TypePrimary submission
Project Data TypeEpigenomics, Transcriptome or Gene Expression

General info

Project titleb-catenin-mediated upregulation of the ASBEL-TCF3 complex is critical for tumorigenicity of colon cancer cells
Project 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.
Release Date2016-10-08

Project Type

Sample scope/Material/Capture/Methodology

Sample ScopeMultiisolate
MaterialTranscriptome
CaptureWhole
MethodologySequencing

Objective

ObjectiveSequence, Expression

Target

Organism information

Organism nameHomo sapiens
Taxonomy ID9606