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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	non small cell lung cancer
ICD-0-3	C34
Methods	qPCR, Western blot, in vitro knockdown, etc.
Sample	NSCLC tissue, human NSCLC cell lines A549, H1299 and NCIH460 and normal human bronchial epithelial cell line 16HBE
Expression Pattern	up-regulated
Function Description	MIR31HG was significantly increased in tumor tissues compared with adjacent normal tissues, and increased MIR31HG expression levels were associated with histological differentiation grade, lymph node metastasis and Tumor node metastasis (TNM) stage in patients with NSCLC. Patients who had a higher MIR31HG expression level, were predicted a shorter over survival (OS) time. Using in vitro assays, the present study demonstrated that the downregulation of MIR31HG expression significantly inhibited cell proliferation and cell invasion abilities. Furthermore, it was identified that knockdown of MIR31HG expression suppressed the cell epithelial mesenchymal transition (EMT) phenotype by reducing the expression levels of Twist1 and Vimentin, but also increased the expression level of E cadherin in NSCLC cells. Furthermore, the results of the present study demonstrated that downregulated MIR31HG inhibited the Wnt/? catenin signaling pathway by decreasing the expression of glycogen synthase kinase 3? (GSK3?) and ? catenin, but increasing the phosphorylated (p) GSK3? expression in NSCLC cells.
Pubmed ID	30655759
Year	2019
Title	MIR31HG promotes cell proliferation and invasion by activating the Wnt/?-catenin signaling pathway in non-small cell lung cancer

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