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MicroRNA-145 induces apoptosis of glioma cells by targeting BNIP3 and Notch signaling.

作者信息

Du Yan, Li Juan, Xu Tao, Zhou Dan-Dan, Zhang Lei, Wang Xiao

机构信息

School of Pharmacy, Anhui Province Key Laboratory of Major Autoimmune Diseases, Anhui Institute of Innovative Drugs, Anhui Medical University, Hefei 230032, China.

Institute for Liver Disease of Anhui Medical University, Anhui Medical University, Hefei 230032, China.

出版信息

Oncotarget. 2017 Jun 22;8(37):61510-61527. doi: 10.18632/oncotarget.18604. eCollection 2017 Sep 22.


DOI:10.18632/oncotarget.18604
PMID:28977881
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5617441/
Abstract

MicroRNAs (miRNAs) are involved in the pathogenesis of various human cancers. Here we show that miR-145 expression is decreased in human glioma samples, rat glioma tissues, and glioma cell lines, while expression of BNIP3 is increased. Over-expression of miR-145 or suppression of BNIP3 induced glioma cell apoptosis. BNIP3 is localized in the nucleus in glioma cells, and miR-145 inhibits BNIP3 expression by binding to the 3' untranslated region of its mRNA. Interestingly, miR-145 and BNIP3 regulate glioma cell apoptosis by modulating Notch signaling. These results indicate that miR-145 increases glioma cell apoptosis by inhibiting BNIP3 and Notch signaling, and suggest that miR-145 may serve as a novel therapeutic target for malignant glioma.

摘要
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2323/5617441/d94baffa6067/oncotarget-08-61510-g012.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2323/5617441/ae599c911bc7/oncotarget-08-61510-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2323/5617441/59dbd266c70b/oncotarget-08-61510-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2323/5617441/ce48c53780cd/oncotarget-08-61510-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2323/5617441/2f8ef39f15ef/oncotarget-08-61510-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2323/5617441/f10f823c692d/oncotarget-08-61510-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2323/5617441/8ccf9f22b37d/oncotarget-08-61510-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2323/5617441/be4421b3be4b/oncotarget-08-61510-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2323/5617441/878e5e4886cd/oncotarget-08-61510-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2323/5617441/64e8d44d56fe/oncotarget-08-61510-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2323/5617441/b377737ddad3/oncotarget-08-61510-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2323/5617441/86a1af7964f8/oncotarget-08-61510-g011.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2323/5617441/d94baffa6067/oncotarget-08-61510-g012.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2323/5617441/ae599c911bc7/oncotarget-08-61510-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2323/5617441/59dbd266c70b/oncotarget-08-61510-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2323/5617441/ce48c53780cd/oncotarget-08-61510-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2323/5617441/2f8ef39f15ef/oncotarget-08-61510-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2323/5617441/f10f823c692d/oncotarget-08-61510-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2323/5617441/8ccf9f22b37d/oncotarget-08-61510-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2323/5617441/be4421b3be4b/oncotarget-08-61510-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2323/5617441/878e5e4886cd/oncotarget-08-61510-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2323/5617441/64e8d44d56fe/oncotarget-08-61510-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2323/5617441/b377737ddad3/oncotarget-08-61510-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2323/5617441/86a1af7964f8/oncotarget-08-61510-g011.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2323/5617441/d94baffa6067/oncotarget-08-61510-g012.jpg

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[9]
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[4]
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[5]
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[6]
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[7]
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[8]
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J Cancer. 2022-2-28

[9]
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[10]
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本文引用的文献

[1]
MiR-199b-5p inhibits osteogenic differentiation in ligamentum flavum cells by targeting JAG1 and modulating the Notch signalling pathway.

J Cell Mol Med. 2017-6

[2]
Targeting the Notch-regulated non-coding RNA TUG1 for glioma treatment.

Nat Commun. 2016-12-6

[3]
miR-92a-3p Exerts Various Effects in Glioma and Glioma Stem-Like Cells Specifically Targeting CDH1/β-Catenin and Notch-1/Akt Signaling Pathways.

Int J Mol Sci. 2016-10-27

[4]
MicroRNA-93 Downregulation Ameliorates Cerebral Ischemic Injury Through the Nrf2/HO-1 Defense Pathway.

Neurochem Res. 2016-10

[5]
MicroRNA-145 inhibits hepatic stellate cell activation and proliferation by targeting ZEB2 through Wnt/β-catenin pathway.

Mol Immunol. 2016-7

[6]
iNOS Induces Vascular Endothelial Cell Migration and Apoptosis Via Autophagy in Ischemia/Reperfusion Injury.

Cell Physiol Biochem. 2016

[7]
Auricular vagus nerve stimulation promotes functional recovery and enhances the post-ischemic angiogenic response in an ischemia/reperfusion rat model.

Neurochem Int. 2016-7

[8]
MiR-129 triggers autophagic flux by regulating a novel Notch-1/ E2F7/Beclin-1 axis to impair the viability of human malignant glioma cells.

Oncotarget. 2016-2-23

[9]
Shikonin Inhibits the Migration and Invasion of Human Glioblastoma Cells by Targeting Phosphorylated β-Catenin and Phosphorylated PI3K/Akt: A Potential Mechanism for the Anti-Glioma Efficacy of a Traditional Chinese Herbal Medicine.

Int J Mol Sci. 2015-10-9

[10]
Bcl-2 family member Mcl-1 expression is reduced under hypoxia by the E3 ligase FBW7 contributing to BNIP3 induced cell death in glioma cells.

Cancer Biol Ther. 2016-6-2

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