MiR-9 inhibits childhood leukemia cell apoptosis via regulating notch signaling pathway

Osteosarcoma (OS) is the most common histological form of primary bone cancer. It is most prevalent in teenagers and young adults. The present study aims at exploring the regulatory effect of microRNA-340 (miR-340) on OS cell proliferation, invasion, migration, and apoptosis via regulating the Notch signaling pathway by targeting β-catenin (cadherin-associated protein) 1 (CTNNB1). OS tissues belonging to 45 patients and normal femoral head tissues of 45 amputees were selected. Cells were allocated to different groups. In situ hybridization was performed to determine the positive rate of miR-340 expression while immunohistochemistry was used to determine that of CTNNB1 and B-cell lymphoma 2 (Bcl-2). We used a series of experiments to measure the expressions of related factors and assess rates of cell proliferation, migration, invasion, cycle, and apoptosis respectively. Our results show that miR-340 was expressed a higher level in normal tissue than OS tissue. Expression of Notch, CTNNB1, hairy and enhancer of split 1 (Hes1), Bcl-2, Runt-related transcription factor 2 (Runx2), and osteocalcin increased and that of miR-340, Bcl-2 interacting mediator of cell death (BIM), and Bcl-2 associated protein X (Bax) decreased in OS tissues. U-2OS cell line had the highest miR-340 expression. We also found that the up-regulation of miR-340 had increased expression of miR-340, BIM, and Bax but decreased expression of Notch, CTNNB1, Hes1, Bcl-2, Runx2, and osteocalcin. Up-regulation of miR-340p lead to increased cell apoptosis, suppressed cell proliferation, migration, and invasion. Our study demonstrates that overexpression of miR-340 could suppress OS cell proliferation, migration, and invasion as well as promoting OS cell apoptosis by inactivating the Notch signaling pathway via down-regulating CTNNB1. Functional miR-340 overexpression might be a future therapeutic strategy for OS.

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Corrigendum to “Down-regulation of UBA6 exacerbates brain injury by inhibiting the activation of Notch signaling pathway to promote cerebral cell apoptosis in rat acute cerebral infarction model” [Mol. Cell. Probes 53 (2020) 101612]

Molecular and Cellular Probes ◽

10.1016/j.mcp.2021.101773 ◽

2021 ◽

pp. 101773

Author(s):

Zhiguo Chen ◽

Jiangang Liu ◽

Qingmei Chen ◽

Min Su ◽

Haifeng Lu ◽

...

Keyword(s):

Brain Injury ◽

Cerebral Infarction ◽

Notch Signaling ◽

Signaling Pathway ◽

Cell Apoptosis ◽

Notch Signaling Pathway ◽

Acute Cerebral Infarction ◽

Down Regulation

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EGFL7 silencing inactivates the Notch signaling pathway; enhancing cell apoptosis and suppressing cell proliferation in human cutaneous melanoma

Neoplasma ◽

10.4149/neo_2018_180310n167 ◽

2019 ◽

Vol 66 (02) ◽

pp. 187-196 ◽

Cited By ~ 1

Author(s):

H. Tang ◽

W. R. Xiao ◽

Y. Y. Liao ◽

L. Li ◽

X. Xiao ◽

...

Keyword(s):

Cell Proliferation ◽

Notch Signaling ◽

Signaling Pathway ◽

Cutaneous Melanoma ◽

Cell Apoptosis ◽

Notch Signaling Pathway

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MicroRNA-384-5p Promotes Endothelial Progenitor Cell Proliferation and Angiogenesis in Cerebral Ischemic Stroke through the Delta-Likeligand 4-Mediated Notch Signaling Pathway

Cerebrovascular Diseases ◽

10.1159/000503950 ◽

2020 ◽

Vol 49 (1) ◽

pp. 39-54 ◽

Cited By ~ 5

Author(s):

Jia Fan ◽

Weiwei Xu ◽

Shanji Nan ◽

Meiji Chang ◽

Yizhi Zhang

Keyword(s):

Cell Proliferation ◽

Ischemic Stroke ◽

Infarct Size ◽

Notch Signaling ◽

Signaling Pathway ◽

Cell Apoptosis ◽

Notch Signaling Pathway ◽

Brain Infarct ◽

Cerebral Ischemic Stroke ◽

Cerebral Ischemic

Background: MicroRNAs (miRs) have a crucial regulatory role in endothelial cell function and tumor angiogenesis by inhibiting the expressions of their target genes. The participation of microRNA-384-5p (miR-384-5p) has been prominently reported in various ischemia-induced diseases such as myocardial ischemia and atherosclerosis. Hence, the present study aimed at exploring the effect of miR-384-5p on proliferation, apoptosis, and angiogenesis of endothelial progenitor cells (EPCs) in cerebral ischemic stroke and investigating the associated underlying mechanism. Methods: A middle cerebral artery occlusion (MCAO) mouse model was established, with determination of the expression of cluster of differentiation 31 (CD31) and vascular endothelial growth factor (VEGF) proteins. Next, the MCAO mice and EPCs separated from MCAO mice were injected or transfected with mimics or inhibitors of miR-384-5p, or small interference RNA Delta-likeligand 4 (si-DLL4) in order to evaluate their effect on brain infarct size, cell proliferation, apoptosis, and angiogenesis. The relationship among miR-384-5p, DLL4, and the Notch signaling pathway was then verified by a series of experiments. Results: In MCAO mice, an increased brain infarct size and cell apoptosis in brain tissues were evident, with decreased expression of miR-384-5p, VEGF, and CD31, as well as increased DLL4 expression. After miR-384-5p mimic or si-DLL4 treatment, the brain infarct size and cell apoptosis in the brain tissues were reduced in compliance with an increased expression of VEGF and CD31. Our findings demonstrated that miR-384-5p negatively regulated the expression of DLL4, which further downregulated the Notch signaling pathway. When miR-384-5p was overexpressed or DLL4 silenced, the cell proliferation and angiogenesis of EPCs were promoted and cell apoptosis was inhibited. Conclusions: Our study demonstrated that overexpressed miR-384-5p targeting DLL4 could stimulate proliferation and angiogenesis, while inhibiting apoptosis of EPCs in mice with cerebral ischemic stroke through the Notch signaling pathway.

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