Long non‑coding RNA MEG3 suppresses the growth of glioma cells by regulating the miR‑96‑5p/MTSS1 signaling pathway

Zhang, Shoudan; Guo, Wei

doi:10.3892/mmr.2019.10659

Cited by 30 publications

(32 citation statements)

References 48 publications

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“…Subsequently, lncRNA MEG3 expression was found to be downregulated in glioma tissue cells. Zhang et al (10) reported that lncRNA MEG3 inhibited glioma cell growth in vitro by regulating the mir-96-5p/MTSS1 signaling pathway, and was involved in cell proliferation and apoptosis regulation. Earlier studies indicated that lncRNA MEG3 also showed a downregulated trend in the brain tissues of patients with Huntington's disease, and Meg3knockout affected the expression of genes in the cerebral cortex of mice, leading to increased cortical microvascular density and enhanced expression of genes related to angiogenesis (19).…”

Section: Discussionmentioning

confidence: 99%

“…LncRNAs are protein-free transcripts, but occupy a large part of the transcription output. They are involved in the regulation of epigenetic, transcription, and post-transcriptional processing in cell homeostasis, and have attracted increased research attention in biomedicine, with particular focus of the roles of lncRNAs in normal neurodevelopment and neurogenerative diseases (including Alzheimer's disease, Huntington's disease, and PD) (10,11). However, this field is still in its infancy, and the function of most identified lncRNAs remains unclear.…”

Section: Introductionmentioning

confidence: 99%

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Association of the Plasma Long Non-coding RNA MEG3 With Parkinson's Disease

et al. 2020

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Objective: To investigate the expression level of the maternally expressed gene-3 (MEG3) of the free long non-coding RNA (lncRNAs) in the plasma of Parkinson's disease (PD) patients and its relationship with the disease.Methods: Thirty PD patients (PD group) who treated at Xuanwu Hospital of Capital University of Medical Sciences between January 2017 and December 2019 were selected as the research objects and 30 healthy subjects were enrolled in the study during the same period as the control group. Cognitive function was assessed according to the Mini-Mental State Examination (MMSE) and Montreal Cognitive Assessment (MoCA) were used to evaluate cognitive function, Non-Motor Symptoms Scale (NMSS) was used to evaluate severity of non-motor symptoms. The relative expression of lncRNAs MEG3 in plasma was measured by PCR, and the levels of neuron-specific enolase (NSE), nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) in plasma were measured by ELISA, and the relationship with these all indexes was analyzed.Results: The NMSS score of PD group was significantly higher than that of the control group, while the MMSE and MoCA scores were significantly lower than that of the control group (P < 0.05); The relative expression of lncRNAs MEG3, NGF and BDNF levels of PD group were significantly lower than that of the control group, and NSE level was significantly higher than that of the control group (P < 0.05); The H&Y stage and NMSS score in PD group were negatively correlated with the relative expression of lncRNAs MEG3, the levels of NGF and BDNF (P < 0.05), and positively correlated with NSE (P < 0.05); The MMSE and MoCA scores in PD group were positively correlated with the relative expression of lncRNAs MEG3, NGF, BDNF levels (P < 0.05), and negatively correlated with NSE (P < 0.05); The relative expression of lncRNAs MEG3 in PD group was positively correlated with NGF, BDNF levels (P < 0.05), and negatively correlated with NSE (P < 0.05).Conclusion: The expression of lncRNAs MEG3 in the plasma of PD patients was downregulated compared to that of healthy control subjects, and its expression level was closely related to the aggravation of non-motor symptoms, cognitive decline, and PD stage. These associations may reflect the synergism of the increase of NSE and decrease of NGF and BDNF levels, highlighting plasma lncRNA MEG3 as a new candidate biomarker of PD.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Association of the Plasma Long Non-coding RNA MEG3 With Parkinson's Disease

et al. 2020

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“…The role of MEG3 in cancers has been reported in several studies in which the interaction between lncRNAs, miR and mRNA, has been highlighted [26,27]. In glioma, MEG3 inhibited the proliferation, migration and invasion of glioma cells by regulating miR-96-5p/MTSS1 [28].In multiple myeloma, MEG3 inhibited tumor progression through regulating the miR-181a/HOXA11 axis [29].Particularly, previous studies have suggested that MEG3/miR-9-5p is involved in regulating the progression of prostate cancer and esophageal cancer by targeting QKI-5 and FOXO1. Recently, a study by Liu et al found that MEG3 can serve as a ceRNA for miR-9-5p to mediate the development of HCC through upregulating SOX11 [30].To further explore the molecular mechanisms underlying the role of MEG3 in HCC, we investigated whether MEG3 exerts its protective effects in HCC via regulating miR-9-5p/MDK axis.…”

Section: Mmp1 Is Involved In Invasion and Metastasis During The Develmentioning

confidence: 97%

LncRNA MEG3 affects cell proliferation, apoptosis and migration by targeting miR-9-5p/MDK axis and activating PDK/AKT pathway in hepatocellular carcinoma

Wu¹,

Ma²,

Ma³

et al. 2020

Preprint

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KEYWORDShepatocellular carcinoma, lncRNA MEG3, miR-9-5p, MDK, PDK/AKT pathway 2 Abstract Background Long non-coding RNA (lncRNA) maternally expressed gene 3 (MEG3) was supposed to be a tumor suppressor in various cancers. However, the role of MEG3 in hepatocellular carcinoma (HCC) and the related molecular mechanisms are not well illustrated. This study aimed to determine the biological function of MEG3 in regulating HCC cell proliferation, apoptosis and migration. Moreover, the interaction among MEG3, microRNA (miR)-9-5p and Midkine (MDK), and the activation of phosphoinositide-dependent kinase (PDK)/AKT pathway in HCC cells were examined. Methods and ResultsExpression of MEG3 in a series of liver cancer cell lines was detected by RT-qPCR. Luciferase reporter assay, RT-qPCR and western blot were used to determine the interaction among MEG3, miR-9-5p and MDK, and the activation of PDK/AKT pathway. Cell proliferation and apoptosis were evaluated by CCK8, flow cytometry analysis for cell cycle and apoptosis, and Caspase 3/9 activity. Cell migration was determined by wound healing assay and MMP1 expression. We found MEG3 was decreased in HCC cell lines compared with the normal liver cell line. MEG3 suppressed HCC cell proliferation and migration, and induced cell apoptosis. Further, we found MEG3 targets miR-9-5p/MDK axis and modulates PDK/AKT pathway in HCC. ConclusionOur findings demonstrated that lncRNA MEG3 affects HCC cell proliferation, apoptosis and migration through its targeting of miR-9-5p/MDK and regulating of PDK/AKT pathway. This study suggested MEG3/miR-9-5p/MDK axis as the potential therapeutic target in HCC.

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“…In addition, downregulation of MEG3 was also observed in human glioma cell lines, compared with normal astrocytes. The promoting effects of miR-96-5p on cell growth and metastasis can be reversed by upregulation of MEG3 [65]. Moreover, Wang et al showed that the expression of MEG3 inhibits cell proliferation and results in G0/G1 arrest in human glioma cell lines through association with p53 [21].…”

Section: Megmentioning

confidence: 99%

Coding of Glioblastoma Progression and Therapy Resistance through Long Noncoding RNAs

Zottel

Šamec

Paska

et al. 2020

Cancers

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Glioblastoma is the most aggressive and lethal primary brain malignancy, with an average patient survival from diagnosis of 14 months. Glioblastoma also usually progresses as a more invasive phenotype after initial treatment. A major step forward in our understanding of the nature of glioblastoma was achieved with large-scale expression analysis. However, due to genomic complexity and heterogeneity, transcriptomics alone is not enough to define the glioblastoma “fingerprint”, so epigenetic mechanisms are being examined, including the noncoding genome. On the basis of their tissue specificity, long noncoding RNAs (lncRNAs) are being explored as new diagnostic and therapeutic targets. In addition, growing evidence indicates that lncRNAs have various roles in resistance to glioblastoma therapies (e.g., MALAT1, H19) and in glioblastoma progression (e.g., CRNDE, HOTAIRM1, ASLNC22381, ASLNC20819). Investigations have also focused on the prognostic value of lncRNAs, as well as the definition of the molecular signatures of glioma, to provide more precise tumor classification. This review discusses the potential that lncRNAs hold for the development of novel diagnostic and, hopefully, therapeutic targets that can contribute to prolonged survival and improved quality of life for patients with glioblastoma.

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Long non‑coding RNA MEG3 suppresses the growth of glioma cells by regulating the miR‑96‑5p/MTSS1 signaling pathway

Cited by 30 publications

References 48 publications

Association of the Plasma Long Non-coding RNA MEG3 With Parkinson's Disease

Association of the Plasma Long Non-coding RNA MEG3 With Parkinson's Disease

LncRNA MEG3 affects cell proliferation, apoptosis and migration by targeting miR-9-5p/MDK axis and activating PDK/AKT pathway in hepatocellular carcinoma

Coding of Glioblastoma Progression and Therapy Resistance through Long Noncoding RNAs

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