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Long non-coding RNA ELF3-antisense RNA 1 promotes osteosarcoma cell proliferation by upregulating Kruppel-like factor 12 potentially via methylation of the microRNA-205 gene.

ABSTRACT: A recent study characterized the long non-coding RNA (lncRNA) ELF3-antisense RNA 1 (ELF3-AS1) as an oncogenic lncRNA in bladder cancer. The present study aimed to investigate the role of ELF3-AS1 in osteosarcoma (OS). It was found that ELF3-AS1 was upregulated in OS tissues, and ELF3-AS1 expression level increased with increasing clinical stage. In OS tissues, Kruppel-like factor 12 (KLF12) was positively correlated with ELF3-AS1, while microRNA (miR)-205 was negatively correlated with ELF3-AS1. ELF3-AS1 overexpression resulted in the upregulation of KLF12, but the downregulation of miR-205. Overexpression of miR-205 caused downregulation of KLF12, but had no significant effects on ELF3-AS1 expression. Overexpression of KLF12 showed no significant impact on ELF3-AS1 and miR-205. ELF3-AS1 and KLF12 overexpression resulted in an increased proliferation rate in OS cells, while miR-205 played an opposite role and attenuated the effects of ELF3-AS1 overexpression. ELF3-AS1 overexpression promoted the methylation of the miR-205 gene. Therefore, ELF3-AS1 may promote OS cell proliferation by upregulating KLF12 through the methylation of the miR-205 gene.

SUBMITTER: Yuan J

PROVIDER: S-EPMC7039168 | biostudies-literature | 2020 Mar

REPOSITORIES: biostudies-literature

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Long non-coding RNA ELF3-antisense RNA 1 promotes osteosarcoma cell proliferation by upregulating Kruppel-like factor 12 potentially via methylation of the microRNA-205 gene.

Yuan Jianmin J Kang Jianhui J Yang Min M

Oncology letters 20200116 3

A recent study characterized the long non-coding RNA (lncRNA) ELF3-antisense RNA 1 (ELF3-AS1) as an oncogenic lncRNA in bladder cancer. The present study aimed to investigate the role of ELF3-AS1 in osteosarcoma (OS). It was found that ELF3-AS1 was upregulated in OS tissues, and ELF3-AS1 expression level increased with increasing clinical stage. In OS tissues, Kruppel-like factor 12 (KLF12) was positively correlated with ELF3-AS1, while microRNA (miR)-205 was negatively correlated with ELF3-AS1. ...[more]

PMID: 32194747

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Project description:Background:Osteosarcoma (OS) is the most common primary malignancy of bone with a high incidence in children. Circular RNAs (circRNAs) play crucial roles in the carcinogenesis and chemoresistance of OS. In the current work, we focused on the function and mechanism of hsa_circ_0003496 (circ_0003496) in OS progression and chemoresistance. Materials and Methods:The expression levels of circ_0003496, miR-370 and Krüppel-like factor 12 (KLF12) mRNA were measured by quantitative real-time polymerase chain reaction (qRT-PCR). The Cell Counting Kit-8 (CCK-8) assay was used to assess the 50% inhibitory concentration (IC50) value and cell proliferation. Cell migration, invasion and apoptosis were detected by transwell assay and flow cytometry, respectively. Western blot analysis was performed to assess the protein level. Targeted relationships among circ_0003496, miR-370 and KLF12 were validated by dual-luciferase reporter, RNA immunoprecipitation (RIP) and RNA pull-down assays. Animal studies were carried out to observe the role of circ_0003496 in vivo. Results:Our results indicated that circ_0003496 up-regulation was associated with doxorubicin (DXR) resistance of OS. Circ_0003496 knockdown repressed DXR-resistant OS cell proliferation, migration and invasion, and enhanced apoptosis and DXR sensitivity. Circ_0003496 functioned as a sponge of miR-370, and miR-370 mediated the regulatory effect of circ_0003496 depletion on DXR-resistant OS cell progression and DXR sensitivity. KLF12 was a direct target of miR-370, and miR-370 overexpression suppressed cell progression and enhanced DXR sensitivity by KLF12. Moreover, circ_0003496 protected against KLF12 repression through sponging miR-370. Additionally, circ_0003496 knockdown hampered tumor growth and promoted DXR sensitivity in vivo. Conclusion:Our present work suggested that the knockdown of circ_0003496 suppressed OS progression and enhanced DXR sensitivity at least partially through modulating KLF12 expression via functioning as a miR-370 sponge, highlighting new opportunities for OS management.

Project description:AimsEpicardium and epicardium-derived cells are critical players in myocardial fibrosis. Mesenchymal stem cell-derived extracellular vesicles (EVs) have been studied for cardiac repair to improve cardiac remodelling, but the actual mechanisms remain elusive. The aim of this study is to investigate the mechanisms of EV therapy for improving cardiac remodelling and develop a promising treatment addressing myocardial fibrosis.Methods and resultsExtracellular vesicles were intrapericardially injected for mice myocardial infarction treatment. RNA-seq, in vitro gain- and loss-of-function experiments, and in vivo studies were performed to identify targets that can be used for myocardial fibrosis treatment. Afterward, a lipid nanoparticle-based long non-coding RNA (lncRNA) therapy was prepared for mouse and porcine models of myocardial infarction treatment. Intrapericardial injection of EVs improved adverse myocardial remodelling in mouse models of myocardial infarction. Mechanistically, Tcf21 was identified as a potential target to improve cardiac remodelling. Loss of Tcf21 function in epicardium-derived cells caused increased myofibroblast differentiation, whereas forced Tcf21 overexpression suppressed transforming growth factor-β signalling and myofibroblast differentiation. LncRNA-Tcf21 antisense RNA inducing demethylation (TARID) that enriched in EVs was identified to up-regulate Tcf21 expression. Formulated lncRNA-TARID-laden lipid nanoparticles up-regulated Tcf21 expression in epicardium-derived cells and improved cardiac function and histology in mouse and porcine models of myocardial infarction.ConclusionThis study identified Tcf21 as a critical target for improving cardiac fibrosis. Up-regulating Tcf21 by using lncRNA-TARID-laden lipid nanoparticles could be a promising way to treat myocardial fibrosis. This study established novel mechanisms underlying EV therapy for improving adverse remodelling and proposed a lncRNA therapy for cardiac fibrosis.

Dataset Information

Long non-coding RNA ELF3-antisense RNA 1 promotes osteosarcoma cell proliferation by upregulating Kruppel-like factor 12 potentially via methylation of the microRNA-205 gene.

Publications

Long non-coding RNA ELF3-antisense RNA 1 promotes osteosarcoma cell proliferation by upregulating Kruppel-like factor 12 potentially via methylation of the microRNA-205 gene.

Similar Datasets

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