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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	acute myeloid leukemia
ICD-0-3	NA
Methods	qPCR, Western blot, Luciferase reporter assay
Sample	Human AML cell lines including Kasumi-1 and AML-193, and a normal human normal BM cell line HS-5, bone marrow
Expression Pattern	up-regulated
Function Description	LINC00662 was significantly increased in AML tissues and cell lines. Knockdown of LINC00662 significantly reduced the growth of AML cells and upregulated AML cell apoptosis. In contrast, overexpression of LINC00662 promoted AML cell growth. MicroRNA-340-5p (miR-340-5p) was predicted as a target of LINC00662. Luciferase reporter assays and RNA pull-down assays confirmed that LINC00662 directly interacted with miR-340-5p. Expression of miR-340-5p was downregulated in AML and silencing of LINC00662 upregulated miR-340-5p expression in AML cells. Moreover, overexpression of miR-340-5p inhibited cell growth and increased apoptosis in AML cells. Inhibition of miR-340-5p significantly reversed the inhibitory effect of LINC00662 silencing on AML cell growth. In addition, Rho-associated protein kinase 1 (ROCK1) was verified as a target gene of miR-340-5p in AML cells. Restoration of ROCK1 expression partially reversed LINC00662 silencing or miR-340-5p overexpression-mediated inhibitory effect on AML cell growth.
Pubmed ID	31306637
Year	2019
Title	High expression of long intergenic non-coding RNA LINC00662 contributes to malignant growth of acute myeloid leukemia cells by upregulating ROCK1 via sponging microRNA-340-5p

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