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Basic Information

Classification Information

Regulatory Mechanism		Biological Function		Clinical Application
TF		Immune		Survival
Enhancer		Apoptosis	apoptosis	Drug
Variant		Cell Growth	3	Circulating
MiRNA		EMT	3	Metastasis
Methylation		Coding Ability		Recurrence

Cancer&Entry Information

Cancer Name	endometrial cancer
ICD-0-3	NA
Methods	qPCR, Western blot, Luciferase reporter assay, in vitro knockdown, etc.
Sample	EC tissues, EC cell lines RL95, HEC1A, AN3CA, and Ishakawa and the immortalized human endometrial epithelial cell line EM-ER-A
Expression Pattern	up-regulated
Function Description	The expression of Lnc-ATB is up-regulated in tumor tissues and EC cell lines. Patients with high expressed Lnc-ATB have high FIGO stage and poor tumor differentiation. The tumor suppressor miR-126 interacted with Lnc-ATB. Down-regulated miR-126 negative correlated with FIGO stage and tumor differentiation. Knockdown of Lnc-ATB in RL95 and HEC1A cell lines increased the miR-126 level and impaired the cell vitality, induced caspase-3-related tumor apoptosis and G1/S arrest. However, abrogation of miR-126 by its inhibitors counteracted Lnc-ATB knockdown-induced tumor inhibition via regulation of miR-126 target gene PIK3R2 and Sox2-related apoptosis and cell cycle pathway. Meanwhile, Lnc-ATB knockdown also suppressed the migration and invasion and inhibited TGF-b-induced epithelial-mesenchymal transition (EMT) phenotype via miR-126. Knockdown of Lnc-ATB in vivo remarkably induced tumor regression via restoration of tumor suppressor miR-126, leading to deceased tumor volume, reduced expression of PCNA and PIK3R2/ Sox2 signals and EMT phenotype in tumor tissues.
Pubmed ID	30601064
Year	2019
Title	Long Noncoding RNA-ATB Impairs the Function of Tumor Suppressor miR-126-Mediated Signals in Endometrial Cancer for Tumor Growth and Metastasis

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