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Updated: Jan 30, 2026
Author Spotlight: RNA FISH for Locating lncRNA-SNHG6 in Osteosarcoma Cells
Published on: June 16, 2023
Long non-coding RNA EPIC1 inhibits viability and invasion of osteosarcoma cells by promoting MEF2D ubiquitylation
Wei Zhao1, Da Zhang1, Pan Qin1
1Department of Pediatric Surgery, The First Affiliated Hospital of Zhengzhou University, No.1 Jianshe East Road, Erqi District, Zhengzhou, Henan 450052, China.
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.
Insights
Overexpression of the long non-coding RNA EPIC1 inhibits osteosarcoma (OS) cell viability and invasion. This occurs by promoting MEF2D protein ubiquitylation, offering new therapeutic targets for OS treatment.
Area of Science:
- Molecular Biology
- Oncology
- Genetics
Background:
- Long non-coding RNAs (lncRNAs) regulate gene expression via diverse mechanisms.
- The specific molecular roles of EPIC1 in osteosarcoma (OS) remain largely unelucidated.
Purpose of the Study:
- To investigate the functional role of EPIC1 in osteosarcoma.
- To explore the molecular mechanism linking EPIC1 and MEF2D in OS development.
Main Methods:
- Quantitative real-time PCR and western blotting to assess EPIC1 and MEF2D expression in OS tissues and cell lines.
- In vitro assays (MTT, transwell) to evaluate cell viability and invasion.
- In vivo studies using an OS xenograft mouse model.
- RNA pull-down and RNA immunoprecipitation (RIP) assays to confirm interactions.
Main Results:
- EPIC1 expression was significantly downregulated, while MEF2D was upregulated in OS tissues and cell lines.
- Overexpression of EPIC1 suppressed OS cell viability and invasion, and inhibited tumor growth in vivo.
- EPIC1 directly targets MEF2D, promoting its ubiquitylation and degradation.
- Restoration of MEF2D expression reversed the inhibitory effects of EPIC1.
Conclusions:
- EPIC1 functions as a tumor suppressor in osteosarcoma.
- EPIC1 inhibits OS progression by enhancing MEF2D ubiquitylation.
- EPIC1 and MEF2D represent potential therapeutic targets for osteosarcoma treatment.
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