POTEE drives colorectal cancer development via regulating SPHK1/p65 signaling.
Zhiyong ShenXiaochuang FengYuan FangYongsheng LiZhenkang LiYizhi ZhanMingdao LinGuoxin LiYi DingHaijun DengPublished in: Cell death & disease (2019)
Aberrant gene expression plays critical roles in the development of colorectal cancer (CRC). Here we show that POTEE, which was identified as a member E of POTE ankyrin domain family, was significantly upregulated in colorectal tumors and predicted poor overall survival of CRC patients. In CRC cells, POTEE could act as an oncogene and could promote cell growth, cell-cycle progression, inhibit apoptosis, and elevates xenograft tumor growth. Mechanically, we used microarray analysis and identified a POTEE/SPHK1/p65 signaling axis, which affected the biological functions of CRC cells. Further evaluation showed that overexpression of POTEE could increase the protein expression of SPHK1, followed by promoting the phosphorylation and activation of p65 protein. Altogether, our findings suggested a POTEE/SPHK1/p65 signaling axis could promote colorectal tumorigenesis and POTEE might potentially serve as a novel biomarker for the diagnosis and an intervention of colorectal cancer.
Keyphrases
- cell cycle arrest
- cell cycle
- induced apoptosis
- gene expression
- cell proliferation
- end stage renal disease
- cell death
- endoplasmic reticulum stress
- randomized controlled trial
- ejection fraction
- oxidative stress
- chronic kidney disease
- signaling pathway
- dna methylation
- transcription factor
- peritoneal dialysis
- prognostic factors
- free survival
- patient reported