Abstract:
:Angiogenesis is a core hallmark of advanced cancers, especially in lung adenocarcinoma (LUAD). However, the underlying functions and mechanisms of lncRNAs in tumor angiogenesis remain largely unknown. Here we found that linc00665 depletion could markedly depressed proliferation and capillary tube formation of HUVECs in vitro. Mechanistically, linc00665 directly interacted with YB-1 protein, enhanced its stability through inhibiting ubiquitination-dependent proteolysis and stimulated its nuclear translocation in LUAD cells. The accumulated nuclear YB-1 activated expression of ANGPT4, ANGPTL3 and VEGFA by binding to their promoters, contributing to tumor-related angiogenesis in vitro and in vivo. Collectively, we conclude that linc00665 induces tumor-related angiogenesis in LUAD by directly interacting with YB-1 and activating YB-1-ANGPT4/ANGPTL3/VEGFA axis, which provides promising anti-angiogenic targets for cancer therapy.
journal_name
Biochem Biophys Res Communjournal_title
Biochemical and biophysical research communicationsauthors
Cong Z,Diao Y,Li X,Jiang Z,Xu Y,Zhou H,Qiang Y,Wu H,Shen Ydoi
10.1016/j.bbrc.2020.04.108subject
Has Abstractpub_date
2020-06-25 00:00:00pages
545-552issue
2eissn
0006-291Xissn
1090-2104pii
S0006-291X(20)30848-2journal_volume
527pub_type
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journal_title:Biochemical and biophysical research communications
pub_type: 杂志文章
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journal_title:Biochemical and biophysical research communications
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journal_title:Biochemical and biophysical research communications
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journal_title:Biochemical and biophysical research communications
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journal_title:Biochemical and biophysical research communications
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journal_title:Biochemical and biophysical research communications
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journal_title:Biochemical and biophysical research communications
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journal_title:Biochemical and biophysical research communications
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journal_title:Biochemical and biophysical research communications
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更新日期:1994-08-30 00:00:00