当前位置： SCI文献检索 > INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES期刊下所有文献 > Long non-coding RNA EPIC1 inhibits viability and invasion of osteosarcoma cells by promoting MEF2D ubiquitylation.

Long non-coding RNA EPIC1 inhibits viability and invasion of osteosarcoma cells by promoting MEF2D ubiquitylation.

Abstract：

BACKGROUND:Long non-coding RNAs (lncRNAs) can modulate gene expression through different mechanisms, but the fundamental molecular mechanism behind EPIC1 and osteosarcoma (OS) was poorly understood. METHODS:Bone tumor tissues and the matched normal tissues were obtained from 36 OS patients who received tumor resection from 2014 to 2018. The expression of EPIC1 and MEF2D was determined by quantitative real-Time PCR and western blotting. Cell viability and invasion were evaluated by MTT assay and transwell assay. The animal xenograft model was also established. RESULTS:EPIC1 was down-regulated, but MEF2D was up-regulated in OS tissues and OS cell lines. Overexpression of EPIC1 inhibited cell viability and invasion of OS cells. Targeting relationship between EPIC1 and MEF2D was confirmed by RNA pull-down and RNA immunoprecipitation (RIP). The MEF2D protein binding to ubiquitin was significantly increased in OS cells overexpressing EPIC1. The co-transfection with pcDNA-EPIC1 and pcDNA-MEF2D rescued the inhibition of cell viability and invasion caused by the overexpression of EPIC1. Overexpression of EPIC1 suppressed tumor growth in the OS xenograft model. CONCLUSION:Our findings indicated that overexpression of EPIC1 inhibited cell viability and invasion of OS cells by promoting MEF2D ubiquitylation, which provided innovative lncRNA and protein targets for treating OS.

journal_name

Int J Biol Macromol

journal_title

International journal of biological macromolecules

authors

Zhao W,Zhang D,Qin P,Zhang J,Cui X,Gao J,Wang J,Li J

doi

10.1016/j.ijbiomac.2019.01.156

subject

Has Abstract

pub_date

2019-05-01 00:00:00

pages

566-573

eissn

0141-8130

issn

1879-0003

pii

S0141-8130(18)36883-1

journal_volume

128

pub_type

杂志文章

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