Long non-coding RNA linc00665 interacts with YB-1 and promotes angiogenesis in lung adenocarcinoma.

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.

authors

Cong Z,Diao Y,Li X,Jiang Z,Xu Y,Zhou H,Qiang Y,Wu H,Shen Y

doi

10.1016/j.bbrc.2020.04.108

subject

Has Abstract

pub_date

2020-06-25 00:00:00

pages

545-552

issue

2

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(20)30848-2

journal_volume

527

pub_type

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