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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	diffuse large B-cell lymphoma
ICD-0-3	NA
Methods	qPCR, Western blot, Luciferase reporter assay, in vitro knockdown, etc.
Sample	DLBCL tissues, GCB subtype cell line OCI-LY7 and ABC subtype cell line OCILY3, HEK293T cells, Normal B lymphocytes
Expression Pattern	up-regulated
Function Description	SNHG16 was overexpressed in DLBCL tissues and the derived cell lines. SNHG16 knockdown significantly suppressed cell proliferation and cell cycle progression, and it induced apoptosis of DLBCL cells in vitro. Furthermore, silencing of SNHG16 markedly re pressed in vivo growth of OCI LY7 cells. Mechanistically, SNHG16 directly interacted with miR 497 5p by acting as a competing endogenous RNA (ceRNA) and inversely regulated the abundance of miR 497 5p in DLBCL cells. Moreover, the proto on cogene proviral integration site for Moloney murine leukaemia virus 1 (PIM1) was identified as a novel direct target of miR 497 5p. SNHG16 overexpression rescued miR 497 5p induced down regulation of PIM1 in DLBCL cells. Importantly, restora tion of PIM1 expression reversed SNHG16 knockdown induced inhibition of prolif eration, G0/G1 phase arrest and apoptosis of OCI LY7 cells.
Pubmed ID	31483572
Year	2019
Title	Long non-coding RNA SNHG16 promotes proliferation and inhibits apoptosis of diffuse large B-cell lymphoma cells by targeting miR-497-5p/PIM1 axis

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