MiR-222-3p downregulation prompted the migration, invasion and recruitment of endothelial progenitor cells via ADIPOR1 expression increase-induced AMKP activation

Gao, Lingyun; Chen, Mingxiang; Li, Fuping

doi:10.1016/j.mvr.2021.104134

Cited by 7 publications

(6 citation statements)

References 29 publications

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“…On the contrary, the miR‐222‐3p depletion stimulates the proliferation, colony formation, and autophagy of HCC cells (Chen et al, 2020). As similarly reported by Gao et al, miR‐222‐3p silencing can also exacerbate the malignant biological activities of endothelial progenitor cells (Gao et al, 2021). From the aforesaid findings, it is suggested that miR‐222‐3p plays a suppressive role in human cancers.…”

Section: Discussionsupporting

confidence: 56%

Enhancer of zeste homolog 2 exerts functions in gastric cancer development via modulating microRNA‐222‐3p methylation and WEE1 expression

et al. 2022

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Enhancer of zeste homolog 2 (EZH2) has been studied in gastric cancer (GC), while the role of EZH2 in GC via binding to microRNA (miR)-222-3p remains obscure. This research aims to unravel the regulatory mechanism of EZH2 in GC progression via the modulation of miR-222-3p/WEE1 axis. Initially, EZH2, miR-222-3p, and WEE1 levels in GC cells and tissues were examined. Thereafter, constructs altering EZH2, miR-222-3p, or WEE1 expression were transfected into GC cells to determine the malignant behaviors involved in tumorigenesis of GC cells.Finally, the targeting relations among EZH2, miR-222-3p, and WEE1 were validated. EZH2 and WEE1 were upregulated while miR-222-3p was down-regulated in GC tissues and cells. The decreased EZH2, silenced WEE1, or restored miR-222-3p constrained the malignant behaviors involved in tumorigenesis of GC cells. Deletion of miR-222-3p could reverse the effect of silenced EZH2 on suppressing the biological functions of GC cells. EZH2 could bind to the promoter of miR-222-3p, and there was a targeting relationship between miR-222-3p and WEE1. Our study demonstrates that EZH2 promotes GC development via the modulation of miR-222-3p/WEE1 axis, thus providing promising therapeutic targets for GC therapy.

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Section: Discussionsupporting

confidence: 56%

Enhancer of zeste homolog 2 exerts functions in gastric cancer development via modulating microRNA‐222‐3p methylation and WEE1 expression

et al. 2022

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“…Studies have found that endothelial progenitor cells have the ability to enhance neovascularization in the case of ischemia and can exert a therapeutic effect around blocked blood vessels that require reperfusion. In addition, the results of animal experiments confirmed that EPCs derived from peripheral blood or bone marrow have the function of promoting angiogenesis and accelerating the recovery of blood supply in ischemic tissues [15][16][17]. In addition, recent studies have shown that endothelial progenitor cells in peripheral blood also have the function of repairing damaged vascular endothelium, so they can be used as a reservoir for endothelial cells [18].…”

Section: Discussionmentioning

confidence: 86%

Effect of Peptidylarginine Deiminase 4 on Endothelial Progenitor Cell Function in Peripheral Arterial Disease

Pan

Liu

Chen

et al. 2021

Evidence-Based Complementary and Alternative Medicine

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At present, the global prevalence of peripheral arterial disease is increasing year by year, and it has become a worldwide disease. Studies have shown that transplanting endothelial progenitor cells (EPCs) into ischemic tissues can improve the tissue ischemia, thereby having a therapeutic effect on peripheral arterial diseases. This indicates that EPCs play a therapeutic effect in peripheral arterial disease. Recent studies have shown that peptidylarginine deiminase (PAD) is involved in the regulation of epigenetics and its inhibitor Cl-amidine can improve endothelium-dependent vasodilation and significantly reduce the formation of arterial thrombosis. It can also play a role in hematopoietic stem cells that share the same origin with EPCs. Therefore, we speculate that PAD4 may also have an effect on EPCs through a similar mechanism, thereby participating in the damage and repair of peripheral arterial disease. Therefore, we first detected the expression of PAD4 in EPCs of peripheral arterial disease and detected changes in the number and function of endothelial progenitor cells in peripheral blood after injecting the PAD4 inhibitor Cl-amidine into mice. A mouse model of lower limb ischemia was established to explore the effect of PAD4 on the function of EPCs in peripheral arterial disease. The results show that PAD4 is highly expressed in peripheral arterial diseases and the PAD4 inhibitor Cl-amidine can increase the number of EPCs and can treat peripheral arterial diseases by improving the proliferation, migration, and vascularization of EPCs.

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“…Gan et al demonstrated that miR-222-3p suppressed osteogenic differentiation of BMSCs through Insulin-like growth factor 1/extracellular regulated protein kinases pathway [ 32 ]. Gao et al indicated that downregulation of miR-222-3p promoted the migration, invasion, and recruitment of Endothelial progenitor cells by activating ADIPOR1-induced 2-amino-3-methyl-4-ketopentanoic acid signaling pathway [ 33 ]. And several studies also proved that miR-222-3p acts as potential biomarkers in the tumor development.…”

Section: Discussionmentioning

confidence: 99%

Mesenchymal Stem Cell-Derived Exosomal miRNA-222-3p Increases Th1/Th2 Ratio and Promotes Apoptosis of Acute Myeloid Leukemia Cells

Yuan

Tan

Wang

et al. 2023

Analytical Cellular Pathology

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Interferon regulatory factor 2 (IRF2) participates in the differentiation of immune T cells. Bone marrow mesenchymal stem cell (BM-MSC)-derived exosomes can secret mRNA, miRNAs, and proteins to regulate tumor microenvironment. The present study focused on the miRNA/IRF2 axis in regulating Th1/Th2 ratio and cell apoptosis in acute myeloid leukemia (AML). The flow cytometry analysis was performed to examine the Th1/Th2 ratio and AML apoptosis in vivo and in vitro. The contents of Interferon γ (IFN-γ) and Interleukin-4 (IL-4) were measured using enzyme-linked immunosorbent assay. StarBase was used to predict the potential binding site between miR-222-3p and the 3 ′ untranslated region of IRF2. Luciferase reporter assay was applied for validating the combination of miR-222-3p and IRF2. BM-MSC exosomes were successfully isolated. BM-MSC exosomes increased Th1/Th2 ratio and promoted apoptosis of AML cells. Further analysis showed that IRF2 was targeted by miR-222-3p. Overexpression of miR-222-3p promoted Th1/Th2 ratio and AML cell apoptosis. IRF2 partially reversed the effect that is exerted by miR-222-3p on Th1/Th2 ratio and AML cell apoptosis. Overexpression of miR-222-3p promoted Th1/Th2 ratio and caspase 3 expression in vivo. To sum up, miR-222-3p promotes Th1/Th2 ratio and AML cell apoptosis by regulating IRF2 expression, which provided crucial targets for the treatment of AML.

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MiR-222-3p downregulation prompted the migration, invasion and recruitment of endothelial progenitor cells via ADIPOR1 expression increase-induced AMKP activation

Cited by 7 publications

References 29 publications

Enhancer of zeste homolog 2 exerts functions in gastric cancer development via modulating microRNA‐222‐3p methylation and WEE1 expression

Enhancer of zeste homolog 2 exerts functions in gastric cancer development via modulating microRNA‐222‐3p methylation and WEE1 expression

Effect of Peptidylarginine Deiminase 4 on Endothelial Progenitor Cell Function in Peripheral Arterial Disease

Mesenchymal Stem Cell-Derived Exosomal miRNA-222-3p Increases Th1/Th2 Ratio and Promotes Apoptosis of Acute Myeloid Leukemia Cells

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