Notch activation suppresses endothelial cell migration and sprouting via miR-223-3p targeting Fbxw7

Wang, Ruonan; Yang, Ziyan; Liang, Liang; Feng, Xingxing; Che, Bo; Zhang, Xiaoyan; Zheng, Qijun; Yan, Xianchun; Han, Hua

doi:10.1007/s11626-022-00649-y

Cited by 8 publications

(4 citation statements)

References 37 publications

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“…Of note, using a known NOTCH1-dependent miRNA i.e. the miR-223-3p (Table S 1 ; [ 24 , 25 ]) we obtained comparable results in vitro (Fig. S 2 C-E).…”

Section: Resultssupporting

confidence: 51%

Extracellular vesicle microRNAs contribute to Notch signaling pathway in T-cell acute lymphoblastic leukemia

et al. 2022

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T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive T-cell malignancy characterized by genotypically-defined and phenotypically divergent cell populations, governed by adaptive landscapes. Clonal expansions are associated to genetic and epigenetic events, and modulation of external stimuli that affect the hierarchical structure of subclones and support the dynamics of leukemic subsets. Recently, small extracellular vesicles (sEV) such as exosomes were also shown to play a role in leukemia. Here, by coupling miRNome, bulk and single cell transcriptome profiling, we found that T-ALL-secreted sEV contain NOTCH1-dependent microRNAs (EV-miRs), which control oncogenic pathways acting as autocrine stimuli and ultimately promoting the expansion/survival of highly proliferative cell subsets of human T-cell leukemias. Of interest, we found that NOTCH1-dependent EV-miRs mostly comprised members of miR-17-92a cluster and paralogues, which rescued in vitro the proliferation of T-ALL cells blocked by γ-secretase inhibitors (GSI) an regulated a network of genes characterizing patients with relapsed/refractory early T-cell progenitor (ETP) ALLs. All these findings suggest that NOTCH1 dependent EV-miRs may sustain the growth/survival of immunophenotypically defined cell populations, altering the cell heterogeneity and the dynamics of T-cell leukemias in response to conventional therapies.

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“…Of note, using a known NOTCH1-dependent miRNA i.e. the miR-223-3p (Table S 1 ; [ 24 , 25 ]) we obtained comparable results in vitro (Fig. S 2 C-E).…”

Section: Resultssupporting

confidence: 51%

Extracellular vesicle microRNAs contribute to Notch signaling pathway in T-cell acute lymphoblastic leukemia

et al. 2022

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“… 15 We recently identified a panel of miRNAs that mediate the action of Notch signaling in regulating EC proliferation, migration, and sprouting. 19 , 20 , 22 In the present study, miR-342 was found to serve as a mechano-miR and mediated Notch activation-induced EC arterialization. In cultured ECs, FSS upregulated miR-342 and its host gene EVL in a Notch-dependent manner.…”

Section: Discussionsupporting

confidence: 56%

“…A panel of microRNAs (miRNAs) have been found to mediate the effects of shear stress on regulating EC proliferation, migration, and specification, known as mechano-miRs. 18 , 19 We recently investigated the Notch downstream miRNAs in ECs and found that Notch activation downregulates MYC expression to suppress cell-cycle progression at least partly via miR-218-5p, targeting heterogeneous nuclear ribonucleoprotein1 (hnRNPA1) and eyes absent 3 (EYA3). 20 miR-342-5p (denoted miR-342 for convenience) is located in the intron of the Ena-vasodilator-stimulated phosphoprotein-like (EVL) gene and is another Notch downstream miRNA that suppresses EC proliferation and angiogenesis.…”

Section: Introductionmentioning

confidence: 99%

miR-342-5p downstream to Notch enhances arterialization of endothelial cells in response to shear stress by repressing MYC

Zhang¹,

Sun²,

Zhang³

et al. 2023

Molecular Therapy - Nucleic Acids

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“…MiR-652-3p can also limit the Notch ligand Jagged-1 to exert various effects on angiogenesis and immune cell regulation (167). MiR-223-3p has been reported to be a downstream molecule of Notch signaling that modulates the proliferation, differentiation, migration, and sprouting of ECs (168). Notch activation affects miR-223 transcription and enhances cytokine production by macrophages in patients with RA (169).…”

Section: The Regulation Of Notch Signaling During Angiogenesis By Lnc...mentioning

confidence: 99%

The Notch signaling-regulated angiogenesis in rheumatoid arthritis: pathogenic mechanisms and therapeutic potentials

Zhao,

He,

Zhao

et al. 2023

Front. Immunol.

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Angiogenesis plays a key role in the pathological process of inflammation and invasion of the synovium, and primarily drives the progression of rheumatoid arthritis (RA). Recent studies have demonstrated that the Notch signaling may represent a new therapeutic target of RA. Although the Notch signaling has been implicated in the M1 polarization of macrophages and the differentiation of lymphocytes, little is known about its role in angiogenesis in RA. In this review, we discourse the unique roles of stromal cells and adipokines in the angiogenic progression of RA, and investigate how epigenetic regulation of the Notch signaling influences angiogenesis in RA. We also discuss the interaction of the Notch-HIF signaling in RA’s angiogenesis and the potential strategies targeting the Notch signaling to improve the treatment outcomes of RA. Taken together, we further suggest new insights into future research regarding the challenges in the therapeutic strategies of RA.

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Notch activation suppresses endothelial cell migration and sprouting via miR-223-3p targeting Fbxw7

Cited by 8 publications

References 37 publications

Extracellular vesicle microRNAs contribute to Notch signaling pathway in T-cell acute lymphoblastic leukemia

Extracellular vesicle microRNAs contribute to Notch signaling pathway in T-cell acute lymphoblastic leukemia

miR-342-5p downstream to Notch enhances arterialization of endothelial cells in response to shear stress by repressing MYC

The Notch signaling-regulated angiogenesis in rheumatoid arthritis: pathogenic mechanisms and therapeutic potentials

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