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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	osteosarcoma
ICD-0-3	NA
Methods	qPCR, Luciferase reporter assay, in vitro knockdown
Sample	osteosarcoma tisssues, cell lines (MG63, SaOS2, HOS, and 143B)
Expression Pattern	up-regulated
Function Description	The results indicated that high SNHG7 level in OS correlated with high Enneking stage, distant metastasis, and short overall survival time of OS patients. Knockdown of SNHG7 in tumor cells significantly impaired the cell vitality, migration and invasion or TGF-?-induced epithelial-mesenchymal transition (EMT), induced apoptosis, and G1/S arrest via miR-34a. Mechanistically, the targets of miR-34a could be upregulated by SNHG7, including proliferation-related Notch1, apoptosis-related BCL-2, cell cycle-related CDK6, and EMT-related SMAD4. The oncogene role of SNHG7 in vivo was also confirmed and found that knockdown of SNHG7 delayed the tumor growth with increased miR-34a level and Ki-67 level in OS tissues. These findings demonstrated that the LncRNA SNHG7 is upregulated during the development of OS via inhibition of tumor suppressor miR-34s signals.
Pubmed ID	29989838
Year	2018
Title	Long Noncoding RNA SNHG7 Promotes the Tumor Growth and Epithelial-to-Mesenchymal Transition via Regulation of miR-34a Signals in Osteosarcoma

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