Dataset Information

The Long Non-coding RNA MEG3/miR-let-7c-5p Axis Regulates Ethanol-Induced Hepatic Steatosis and Apoptosis by Targeting NLRC5.

ABSTRACT: Ethanol (EtOH)-induced hepatic injury, characterized by hepatic steatosis with apoptosis, causes heavy health burden personally and socially. Long non-coding RNAs (lncRNAs) have been implicated in liver diseases. However, the role of lncRNA maternally expressed gene 3 (MEG3) in EtOH-induced hepatic injury remains unknown. The aim of present study was to assess the function of MEG3 and its functional interaction with miR-let-7c-5p in EtOH-induced hepatic injury. Here, we observed that MEG3 and NLRC5 expression was increased and miR-let-7c-5p expression decreased in EtOH-fed mice and EtOH-induced AML-12 cells. Knockdown of MEG3 contributed to attenuation of EtOH-induced steatosis and apoptosis in AML-12 cells. Also, expression level of MEG3 negatively correlated with miR-let-7c-5p expression and positively correlated with NLRC5 expression. In contrary to MEG3, miR-let-7c-5p overexpression attenuated EtOH-induced steatosis and apoptosis, as well as suppressed EtOH-induced increase in NLRC5 expression. By luciferase reporter assay, we concluded that miR-let-7c-5p directly binds to NLRC5 3'-UTR, thereby negatively regulates NLRC5 expression. Our data suggested that lncRNA MEG3 functions as a competing endogenous RNA for miR-let-7c-5p to regulate NLRC5 expression in EtOH-induced hepatic injury.

SUBMITTER: Wang Q

PROVIDER: S-EPMC5902529 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature

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The Long Non-coding RNA MEG3/miR-let-7c-5p Axis Regulates Ethanol-Induced Hepatic Steatosis and Apoptosis by Targeting NLRC5.

Wang Qin Q Li Mingfang M Shen Zhiming Z Bu Fangtian F Yu Haixia H Pan Xueyin X Yang Yang Y Meng Xiaoming X Huang Cheng C Li Jun J

Frontiers in pharmacology 20180410

Ethanol (EtOH)-induced hepatic injury, characterized by hepatic steatosis with apoptosis, causes heavy health burden personally and socially. Long non-coding RNAs (lncRNAs) have been implicated in liver diseases. However, the role of lncRNA maternally expressed gene 3 (MEG3) in EtOH-induced hepatic injury remains unknown. The aim of present study was to assess the function of MEG3 and its functional interaction with miR-let-7c-5p in EtOH-induced hepatic injury. Here, we observed that MEG3 and NL ...[more]

PMID: 29692724

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Project description:BACKGROUND: Long non-coding RNAs play an important role in tumorigenesis, hence, identification of cancer-associated lncRNAs and investigation of their biological functions and molecular mechanisms are important for understanding the development and progression of cancer. Recently, the downregulation of lncRNA MEG3 has been observed in various human cancers. However, its role in non-small cell lung cancer (NSCLC) is unknown. The aim of this study was to examine the expression pattern of MEG3 in NSCLC and to evaluate its biological role and clinical significance in tumor progression. METHODS: Expression of MEG3 was analyzed in 44 NSCLC tissues and 7 NSCLC cell lines by qRT-PCR. Over-expression approaches were used to investigate the biological functions of MEG3 in NSCLC cells. Bisulfite sequencing was used to investigate DNA methylation on MEG3 expression. The effect of MEG3 on proliferation was evaluated by MTT and colony formation assays, and cell apoptosis was evaluated by Hoechst staining and Flow-cytometric analysis. NSCLC cells transfected with pCDNA-MEG3 were injection into nude mice to study the effect of MEG3 on tumorigenesis in vivo . Protein levels of MEG3 targets were determined by western blot analysis. Differences between groups were tested for significance using Student's t-test (two-tailed). RESULTS: MEG3 expression was decreased in non-small cell lung cancer (NSCLC) tumor tissues compared with normal tissues, and associated with advanced pathologic stage, and tumor size. Moreover, patients with lower levels of MEG3 expression had a relatively poor prognosis. Overexpression of MEG3 decreased NSCLC cells proliferation and induced apoptosis in vitro and impeded tumorigenesis in vivo. MDM2 and p53 protein levels were affected by MEG3 over-expression in vitro. CONCLUSIONS: Our findings indicate that MEG3 is significantly down-regulated in NSCLC tissues that could be affected by DNA methylation, and regulates NSCLC cell proliferation and apoptosis, partially via the activition of p53. Thus, MEG3 may represent a new marker of poor prognosis and is a potential therapeutic target for NSCLC intervention.

Dataset Information

The Long Non-coding RNA MEG3/miR-let-7c-5p Axis Regulates Ethanol-Induced Hepatic Steatosis and Apoptosis by Targeting NLRC5.

Publications

The Long Non-coding RNA MEG3/miR-let-7c-5p Axis Regulates Ethanol-Induced Hepatic Steatosis and Apoptosis by Targeting NLRC5.

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