The contribution of activating transcription factor 3 to apoptosis of human colorectal cancer cells by protocatechualdehyde, a naturally occurring phenolic compound

2014 ◽  
Vol 564 ◽  
pp. 203-210 ◽  
Author(s):  
Jeong Rak Lee ◽  
Man Hyo Lee ◽  
Hyun Ji Eo ◽  
Gwang Hun Park ◽  
Hun Min Song ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Transcription Factor ◽  
Cancer Cells ◽  
Phenolic Compound ◽  
Activating Transcription Factor 3 ◽  
Human Colorectal Cancer ◽  
Naturally Occurring ◽  
Colorectal Cancer Cells ◽  
Activating Transcription Factor ◽  
Human Colorectal Cancer Cells

scholarly journals ASBEL–TCF3 complex is required for the tumorigenicity of colorectal cancer cells

2016 ◽  
Vol 113 (45) ◽  
pp. 12739-12744 ◽  
Author(s):  
Kenzui Taniue ◽  
Akiko Kurimoto ◽  
Yasuko Takeda ◽  
Takeshi Nagashima ◽  
Mariko Okada-Hatakeyama ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Transcription Factor ◽  
Cancer Cells ◽  
Noncoding Rna ◽  
Cancer Development ◽  
Activating Transcription Factor 3 ◽  
Colorectal Cancer Cells ◽  
Activating Transcription Factor ◽  
Atf3 Expression ◽  
Transcription Factor 3

Wnt/β-catenin signaling plays a key role in the tumorigenicity of colon cancer. Furthermore, it has been reported that lncRNAs are dysregulated in several steps of cancer development. Here we show that β-catenin directly activates the transcription of the long noncoding RNA (lncRNA) ASBEL [antisense ncRNA in the ANA (Abundant in neuroepithelium area)/BTG3 (B-cell translocation gene 3) locus] and transcription factor 3 (TCF3), both of which are required for the survival and tumorigenicity of colorectal cancer cells. ASBEL interacts with and recruits TCF3 to the activating transcription factor 3 (ATF3) locus, where it represses the expression of ATF3. Furthermore, we demonstrate that ASBEL–TCF3–mediated down-regulation of ATF3 expression is required for the proliferation and tumorigenicity of colon tumor cells. ATF3, in turn, represses the expression of ASBEL. Our results reveal a pathway involving an lncRNA and two transcription factors that plays a key role in Wnt/β–catenin–mediated tumorigenesis. These results may provide insights into the variety of biological and pathological processes regulated by Wnt/β-catenin signaling.

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