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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	laryngeal cancer
ICD-0-3	C32
Methods	qPCR, Western blot, Luciferase reporter assay
Sample	293T cells, human bronchial epithelial cells 16HBE, TU212 and TU686, LC tissues and paired adjacent noncancerous laryngeal tissues
Expression Pattern	up-regulated
Function Description	increased SNHG3 in LC tissues and cell lines. Loss of function of SNHG3 reduced cell viability, migration, and invasion of TU212 and TU686 cells. Western blot analyses demonstrated that the protein levels of MMP2 and MMP9 decreased after SNHG3 silencing. Additionally, bioinformatics software predicted that SNHG3 could sponge miR-384 at the 3??UTR with complementary binding sites, which was validated by a dual-luciferase reporter assay. RT-PCR analysis revealed that knockdown of SNHG3 upregulated miR-384 expression and that overexpression of miR-384 decreased SNHG3. Furthermore, a dual-luciferase reporter assay showed that miR-384 could bind to the 3??UTR of WEE1, and inhibition of miR-384 markedly increased WEE1 expression. The mRNA and protein levels of WEE1 were downregulated upon deletion of SNGH3. Suppression of WEE1 partly abolished the tumorigenic migration and invasion potential of the miR-384 inhibitor in migration and invasion. Inhibition of miR-384 partially reversed the biological activities of SNHG3 in TU212 and TU686 cells.
Pubmed ID	31238052
Year	2019
Title	LncRNA SNHG3 regulates laryngeal carcinoma proliferation and migration by modulating the miR-384/WEE1 axis

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