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Table 1 LncRNAs involved in the development of myeloid cells

From: Long non-coding RNAs in the regulation of myeloid cells

LncRNAs

Model system

Observation

Refs

LncRNAs in erythrocytes and megakaryocytes

 LincRNA-EPS

Mouse Ter119+ cells

LincRNA-EPS regulates apoptosis during the terminal differentiation of erythroid cells and blocks the proliferation of erythroid progenitors partly through inhibiting Pycard expression

[35, 37]

 Shlnc-EC6

Erythroid progenitor and hematopoietic stem cells (FLEPHSCs) purified from mouse fetal liver

Shlnc-EC6 knockdown results in increased expression of Rac1 and the up-regulated activation of downstream PIP5K which leads to the inhibition of enucleation in cultured mouse fetal erythroblasts

[38]

 AlncRNA-EC7

Differentiating mouse fetal liver red blood cells/K562 cells

AlncRNA-EC7 mediates erythropoiesis partly by regulating enhancer looping to activate the BAND3 locus

[39, 40]

 MONC MIR100HG

Cord-blood (CB) CD34+-HSPCs

MONC/MIR100HG knockdown inhibits leukemic growth of AMKL cell lines and primary patient samples; MONC interferes with hematopoietic lineage decisions and enhances the proliferation of immature erythroid progenitor cells

[41]

LncRNAs in granulocytes

 HOTAIR

Human AML cells

Lung cancer cells

HOTAIR is up-regulated in acute myeloid leukemia and that indicates a poor prognosis; HOTAIR knockdown is capable of inhibiting the proliferation of AML cells

[54, 55]

 HOTAIRM1

ATRA-induced NB4 cells

HOTAIRM1 plays a role in the myelopoiesis through modulation of gene expression in the HOXA cluster and integrin-controlled cell cycle progression

[50, 56]

 NEAT1

Acute promyelocytic leukemia cells

ATRA could not continue to promote the differentiation of granulocytes after NEAT1 blockade

[60]

 HOXA-AS2

ATRA-induced NB4 cells

HOXA-AS2-mediated negative regulation thus contributes to the fine-tuning of apoptosis during myeloid differentiation

[61]

 PVT1

ATRA-induced NB4 cells

Knockdown of PVT1 leads to the suppression of the MYC protein level and impairs the proliferation of APL cells

[62]

 EGO

IL-5 treated CD34+ hematopoietic progenitors

EGO is highly expressed in mature of eosinophils; knockdown of EGO compromises the expression of several proteins that are important for eosinophil development

[63]

 Morrbid

Human/mouse neutrophils, eosinophils and monocytes

Morrbid integrates extracellular signals to control the lifespan of eosinophils, neutrophils, and monocytes through allele-specific suppression of Bcl2l11

[64]

LncRNAs in monocytes and macrophages

 PACER

PMA- and LPS-stimulated human U937 monocytic cell line

PACER is expressed upstream of the Cox2 promoter and positively regulates COX2 production; PACER binds to and drives the release of the repressive p50 dimer of NF-kB from the Cox2 promoter

[67]

 Lnc-MC

Differentiation from monocyte tomacrophage of THP-1, HL-60, HSPCs

Lnc-MC facilitates the monocyte/macrophage differentiation through sequestering miR-199a-5p and alleviating repression on the expression of ACVR1B

[68]

 LincRNA-Cox2

Pam3CSK 4-stimulated mouse bone marrow-derived macrophages

LincRNA-Cox2 suppresses gene expression through interacting with hnRNP-A/B and hnRNP-A2/B1, modulating histone modification and epigenetic chromatin remodeling

[70, 71]

 THRIL

Pam3CSK 4 -stimulated human THP1 macrophages

THRIL knockdown blocks the different expression of multiple inflammatory genes in THP1 macrophages stimulated with Pam3CSK4

[72]

 Lnc-DC

Differentiation of human and mouse dendritic cells

Lnc-DC promotes phosphorylation and activation of STAT3 by blocking its dephosphorylation by SHP1

[73]

 LncRNA-E330013P06

Mouse/human bone marrow macrophages

LncRNA E330013P06 is significantly up-regulated in M2 macrophages and its overexpression induces the expression of pro-inflammatory and pro-atherogenic genes in macrophages

[74]

 TCONS_00019715

Human monocyte-derived macrophages (MDMs) polarized towards M(IFN-γ + LPS) or M(IL-4) phenotypes

TCONS_00019715 knockdown down-regulates the expression of M(IFN-γ + LPS) markers and promotes the expression of M(IL-4) markers in THP-1 cells induced by IFN-γ and LPS

[75]