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Basic Information

Classification Information

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

Cancer&Entry Information

Cancer Name	colorectal cancer
ICD-0-3	C19.9
Methods	Microarray, qPCR, Western blot, Luciferase reporter assay, in vitro knockdown, RIP
Sample	colorectal cancer tissues, cell lines (LoVo, Caco2, HT29, HCT8, HCT116, and SW480)
Expression Pattern	up-regulated
Function Description	The upregulation of FEZF1-AS1 in colorectal cancer, and revealed that increased FEZF1-AS1 expression is associated with poor survival. Functional assays revealed that FEZF1-AS1 promotes colorectal cancer cell proliferation and metastasis. Silencing FEZF1-AS1 expression decreased the number of cells in S phase and increased cell apoptosis, whereas ectopic FEZF1-AS1 expression promoted G1-S cell-cycle progression and inhibited colorectal cancer apoptosis levels compared with control cells. Mechanistically, FEZF1-AS1 could bind and increase the stability of the pyruvate kinase 2 (PKM2) protein, resulting in increased cytoplasmic and nuclear PKM2 levels. Increased cytoplasmic PKM2 promoted pyruvate kinase activity and lactate production (aerobic glycolysis), whereas FEZF1-AS1-induced nuclear PKM2 upregulation further activated STAT3 signaling. In addition, PKM2 was upregulated in colorectal cancer tissues and correlated with FEZF1-AS1 expression and patient survival.Conclusions: Together, these data provide mechanistic insights into the regulation of FEZF1-AS1 on both STAT3 signaling and glycolysis by binding PKM2 and increasing its stability.
Pubmed ID	29914894
Year	2018
Title	LncRNA-FEZF1-AS1 Promotes Tumor Proliferation and Metastasis in Colorectal Cancer by Regulating PKM2 Signaling

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