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Basic Information

Classification Information

Regulatory Mechanism		Biological Function		Clinical Application
TF		Immune		Survival
Enhancer		Apoptosis	apoptosis	Drug	5-azacytidine
Variant		Cell Growth		Circulating
MiRNA		EMT		Metastasis
Methylation		Coding Ability		Recurrence

Cancer&Entry Information

Cancer Name	chronic myeloid leukemia
ICD-0-3	NA
Methods	qPCR, Western blot, Luciferase reporter assay, in vitro knockdown, RIP
Sample	chronic myeloid leukemia bone marrow samples, cell lines (KCL22 and K562)
Expression Pattern	down-regulated
Function Description	MEG3 and PTEN expression were down-regulated, whereas, MDM2, DNMT1 and miR-21 were up-regulated in the accelerated and blast phases of CML. Treated with 5-azacytidine decreased the level of MDM2, DNMT1 and miR21, but increased the level of MEG3 and PTEN. Overexpression of MEG3 and silencing the expression of miR-21 inhibited proliferation and induced apoptosis. MEG3 overexpression and silencing the expression of miR21 influence the levels of MMP-2, MMP-9, bcl-2 and Bax. MEG3 was able to interact with MDM2 and EZH2. MDM2 could interact with DNMT1 and PTEN. MYC and AKT can interact with EZH2. ChIP-seq showed that the promoter of KLF4 and SFRP2 interacts with DNMT1. The BSP results showed significantly decreasedmethylation of the MEG3 promoter CpG after 5-azacytidine treatmentin the KCL22 cells, whereas the methylation change in K562 cells wasnot significant. Thus, we speculated that MEG3 might interact withmethyltransferase, which leads to the methylation of MEG3.
Pubmed ID	29772439
Year	2018
Title	Long Noncoding RNA MEG3 Inhibits Proliferation of Chronic Myeloid Leukemia Cells by Sponging microRNA21

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