MicroRNA-34ainduces transdifferentiation of glioma stem cells into vascular endothelial cells by targeting Notch pathway

Jin, Zaishun; Zhan, Tao; Tao, Jing; Xu, Biao; Zheng, Huizhe; Cheng, Yongxia; Yan, Bin; Wang, Hongwei; Lü, Guoqiang; Lin, Ying; Guo, Shu

doi:10.1080/09168451.2017.1364965

Cited by 21 publications

(22 citation statements)

References 35 publications

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“…Furthermore, we discovered that miR-34a-5p suppressed glioma progression in vitro by targeting the Notch signaling pathway, which was consistent with results that Jin et al ( 2017 ) reported. In addition, Ji et al ( 2008 , 2009 ) found that miR-34 played an important role in cancer stem cell maintenance and survival.…”

Section: Discussionsupporting

confidence: 91%

NFIX Circular RNA Promotes Glioma Progression by Regulating miR-34a-5p via Notch Signaling Pathway

Zhang

Ling

et al. 2018

Front. Mol. Neurosci.

105

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Objective: The present study aimed to explore the association between NFIX circular RNA (circNFIX) and miR-34a-5p in glioma. Furthermore, this study investigated the influence that circNFIX has on glioma progression through the upregulation of NOTCH1 via the Notch signaling pathway by sponging miR-34a-5p.Methods: We applied five methods, CIRCexplorer2, circRNA-finder, CIRI, find-circ and MapSplice2, to screen for circRNAs with differential expression between three glioma tissue samples and three paired normal tissue samples. The GSEA software was used to confirm whether significantly different pathways were activated or inactivated in glioma tissues. The binding sites between circNFIX and miR-34a-5p were confirmed by TargetScan. QRT-PCR and western blot were used to measure the relative expression levels of circNFIX, miR-34a-5p and NOTCH and identify their correlation in glioma. RNA immunoprecipitation (RIP) validated the binding relationship between circNFIX and miR-34a-5p, while the targeted relationship between NOTCH1 and miR-34a-5p was verified by a dual luciferase reporter assay. Cell viability and mobility were examined by a CCK-8 assay and wound healing assay, and a flow cytometry assay was employed to analyze cell apoptosis. The nude mouse transplantation tumor experiment verified that si-circNFIX exerted a suppressive effect on glioma progression in vivo.Results: Twelve circRNAs were differentially expressed between the tissue types. Of those, circNFIX was the sole circRNA to be overexpressed in glioma among the five methods of finding circRNAs. In addition, the Notch signaling pathway was considerably upregulated in tumor tissues compared with the paired normal brain tissues. It was determined that circNFIX acted as a sponge of miR-34a-5p, a miRNA that targeted NOTCH1. Downregulation of circNFIX and upregulation of miR-34a-5p both inhibited cell propagation and migration. Furthermore, a miR-34a-5p inhibitor neutralized the suppressive effect of si-circNFIX on glioma cells. Si-circNFIX and miR-34a-5p mimics promoted cell apoptosis. Moreover, it was demonstrated in vivo that si-circNFIX could suppress glioma growth by regulating miR-34a-5p and NOTCH1.Conclusion: CircNFIX was markedly upregulated in glioma cells. CircNFIX could regulate NOTCH1 and the Notch signaling pathway to promote glioma progression by sponging miR-34a-5p via the Notch signaling pathway. This finding provided a deeper insight into the function of circNFIX in human glioma cancer progression.

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Section: Discussionsupporting

confidence: 91%

NFIX Circular RNA Promotes Glioma Progression by Regulating miR-34a-5p via Notch Signaling Pathway

Zhang

Ling

et al. 2018

Front. Mol. Neurosci.

105

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“…52 DLL1 prevents glioma cells from transdifferentiating into vascular ECs, furtherly maintaining their population. 53 DLL1 or Notch1 silencing inhibits the proliferation and survival of glioma cells, and significantly prolongs the survival of glioma-bearing mice. 52,54 DLL3 expression in IDH mutant gliomas, particularly in 1p/19q co-deleted subsets is higher than that of IDH wild-type glioblastoma.…”

Section: Delta-like Ligands In Gliomasmentioning

confidence: 99%

“…107 Although DLL1 plays an oncogenic role in cancer, its potential tumor-suppressive effects have been identified. With DLL1 interventions, tumor neovascularization is inhibited by the loss of tumor ECs derived from cancer stem cells (CSCs), 53 the inhibition of VEGF-R2-mediated VEGF signaling 108,109 and increased hypoxia and tumor cell necrosis. 108,109 In the hematopoietic environment of tumors, the downregulation of DLL1 impairs T cell development, leading to a loss of anti-tumor T cell responses.…”

Section: Dll1mentioning

confidence: 99%

The Role of DLLs in Cancer: A Novel Therapeutic Target

Xiu

Liu

Kuang

2020

OTT

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Delta-like ligands (DLLs) control Notch signaling. DLL1, DLL3 and DLL4 are frequently deregulated in cancer and influence tumor growth, the tumor vasculature and tumor immunity, which play different roles in cancer progression. DLLs have attracted intense research interest as anti-cancer therapeutics. In this review, we discuss the role of DLLs in cancer and summarize the emerging DLL-relevant targeting methods to aid future studies.

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“…Many factors and pathways have been shown to be important in the regulation of angiogenesis (Casella et al, 2002;Kitamura et al, 2007;Acar et al, 2012;Yang et al, 2017;Ni et al, 2019). Notch-1 is a well-known factor that can alter the level of angiogenesis in various diseases including rheumatoid arthritis (Gao et al, 2012), cancer (Dos Santos et al, 2017;Jin et al, 2017), and psoriasis (Rooney et al, 2014) by regulating downstream genes.…”

Section: Introductionmentioning

confidence: 99%

LncRNA Xist Contributes to Endogenous Neurological Repair After Chronic Compressive Spinal Cord Injury by Promoting Angiogenesis Through the miR-32-5p/Notch-1 Axis

Cheng

et al. 2020

Front. Cell Dev. Biol.

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Endogenous repair after chronic compressive spinal cord injury (CCSCI) is of great clinical interest. Ischemia-hypoxia-induced angiogenesis has been proposed to play an important role during this repair process. Emerging evidence indicates that long non-coding RNAs (lncRNAs) are involved in the pathophysiological processes of various diseases. Here, we identified a lncRNA (Xist; X-inactive specific transcript) with upregulated expression in cervical spine lesions during endogenous neurological repair in CCSCI rats. Therapeutically, the introduction of Xist to rats increased neurological function in vivo as assayed using the Basso, Beattie, and Bresnahan (BBB) score and inclined plane test (IPT). We found that the introduction of Xist enhanced endogenous neurological repair by promoting angiogenesis and microvessel density after CCSCI, while depletion of Xist inhibited angiogenesis and cell sprouting and migration. Mechanistically, Xist promoted angiogenesis by sponging miR-32-5p and modulating Notch-1 expression both in vitro and in vivo. These findings suggest a role of the Xist/miR-32-5p/Notch-1 axis in endogenous repair and provide a potential molecular target for the treatment of ischemia-related central nervous system (CNS) diseases.

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MicroRNA-34ainduces transdifferentiation of glioma stem cells into vascular endothelial cells by targeting Notch pathway

Cited by 21 publications

References 35 publications

NFIX Circular RNA Promotes Glioma Progression by Regulating miR-34a-5p via Notch Signaling Pathway

NFIX Circular RNA Promotes Glioma Progression by Regulating miR-34a-5p via Notch Signaling Pathway

<p>The Role of DLLs in Cancer: A Novel Therapeutic Target</p>

LncRNA Xist Contributes to Endogenous Neurological Repair After Chronic Compressive Spinal Cord Injury by Promoting Angiogenesis Through the miR-32-5p/Notch-1 Axis

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