Search Result

Basic Information

Classification Information

Regulatory Mechanism		Biological Function		Clinical Application
TF		Immune		Survival
Enhancer		Apoptosis		Drug
Variant		Cell Growth		Circulating
MiRNA		EMT		Metastasis
Methylation		Coding Ability		Recurrence

Cancer&Entry Information

Cancer Name	colon cancer
ICD-0-3	C18
Methods	qPCR, Western blot, Luciferase reporter assay, RIP etc.
Sample	colon cancer tissues, cell lines (Hct116, SW1417, SW620, Caco2, SW480, HT29, HCT8 and NCM460)
Expression Pattern	up-regulated
Function Description	We showed that loss of epithelial characteristics and simultaneous gain of mesenchymal features correlated with CYTOR expression. Knockdown of CYTOR attenuated colon cancer cell migration and invasion. Conversely, ectopic expression of CYTOR induced an EMT program and enhanced metastatic properties of colon cancer cells. Mechanistically, the binding of CYTOR to cytoplasmic B-catenin impeded casein kinase 1 (CK1)-induced B-catenin phosphorylation that enabled it to accumulate and translocate to the nucleus. Reciprocally, B-catenin/TCF complex enhanced the transcription activity of CYTOR in nucleus, thus forming a positive feed-forward circuit. Moreover, elevated CYTOR, alone or combined with overexpression of nuclear B-catenin, was predictive of poor prognosis. Our findings suggest that CYTOR promotes colon cancer EMT and metastasis by interacting with B-catenin, and the positive feed-forward circuit of CYTOR-B-catenin might be a useful therapeutic target in antimetastatic strategy.
Pubmed ID	29606502
Year	2018
Title	A Positive Feed-Forward Loop between LncRNA-CYTOR and Wnt/B-Catenin Signaling Promotes Metastasis of Colon Cancer.

External Links