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.
Keywords: Invasion; Long non-coding RNA EPIC1; MEF2D; Osteosarcoma; Ubiquitylation.
Copyright © 2019. Published by Elsevier B.V.