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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	neuroblastoma
ICD-0-3	NA
Methods	qPCR, Western blot, Luciferase reporter assay, in vitro knockdown, etc.
Sample	NB tissues, NB cell lines (SK-N-AS, SK-N-SH, SH-SY5Y, IMR-32, and SK-N-BE(2)-C)
Expression Pattern	up-regulated
Function Description	SNHG7 expression was markedly higher in NB tissues than that in nontumor tissues. Besides, upregulated SNHG7 was greatly correlated with poor overall survival of NB patients. Functionally, the loss of function assays demonstrated that knockdown of SNHG7 inhibited cell proliferation, migration, invasion, and epithelial mesenchymal transition in NB cells. Mechanically, the bioinformatics analysis predicted that miR 653 5p was the shared partner of SNHG7 and signal transducer and activator of transcription 2 (STAT2). Unsurprisingly, we further confirmed that SNHG7 could interact with miR 653 5p and therefore functioned as the ceRNA of STAT2 so as to regulate STAT2 expression in NB cells. Moreover, STAT2 expression was in inverse proportion to miR 653 5p level but in positive proportion to SNHG7 level in NB tissues. Importantly, the repressed NB progression induced by silenced SNHG7 was reversed by STAT2 overexpression or miR 653 5p inhibitors.
Pubmed ID	30623419
Year	2019
Title	Role of SNHG7-miR-653-5p-STAT2 feedback loop in regulating neuroblastoma progression.

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