LncRNA MEG3 inhibits the progression of prostate cancer by modulating miR‐9‐5p/<i>QKI‐5</i> axis

Wu, Meng; Huang, Yanbin; Chen, Tongchang; Wang, Weichao; Yang, Shiguang; Ye, Zhenfeng; Xi, Xiaoqing

doi:10.1111/jcmm.13658

Cited by 136 publications

(116 citation statements)

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“…In this study, to verify the targeting relationship between MEG3, miR-9-5p and MDK, a dual luciferase reporter assay was performed. Consistent with the above reports [9,30], we found MEG3 directly targets miR-9-5p.Subsequently, we demonstrated that MDK is a direct target of miR-9-5p.This finding was in agreement with a previous study reporting that exosomal miR-9 targets MDK in nasopharyngeal carcinoma [15]. Further, we found the expression of miR-9-5p is downregulated, and the expression of MDK is upregulated by MEG3, indicating that MEG3 could regulate the miR-9-5p/MDK axis in HCC.…”

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

confidence: 93%

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

confidence: 93%

“…LncRNAs and miRNAs could interact with each other to serve a wide spectrum of biological functions [7,8]. MEG3 has been reported to serve as a competing endogenous RNA (ceRNA) for miR-9-5p in prostate cancer [9] and esophageal cancer [10] to mediate tumor progression.…”

Section: Introductionmentioning

confidence: 99%

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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show abstract

“…Relevant study has disclosed the interactions among lncRNA, miRNA, and target genes in the study of tumor mechanism. For instance, lncRNA MEG3 could hinder prostate cancer progression via modulating miR-9-5p/QKI-5 axis [28]. LncRNA MEG3 blocks cell proliferation and induces cell apoptosis in laryngeal cancer through regulating miR-23a/APAF-1 axis [29].…”

Section: Discussionmentioning

confidence: 99%

Tumor-Suppressive Function of lncRNA-MEG3 in Glioma Cells by Regulating miR-6088/SMARCB1 Axis

Gong

Huang

2020

BioMed Research International

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Objective. Mounting evidence has elaborated the implication of long noncoding RNAs (lncRNAs) in tumorigenesis of several cancers, including glioma. However, little was known about the mechanism of lncRNA maternally expressed gene 3 (MEG3) in the development and progression of glioma. This work is designed to explore the effect of MEG3 on glioma progression and its possible mechanism. Methods. Expressions of lncRNA-MEG3 and SMARCB1 were detected in human glioblastoma U87 and U251 cell lines. Gain and loss of function of MEG3 or/and miR-6088 was performed in U87 and U251 cells to observe its effect on cell proliferation and migration as well as on epithelial-mesenchymal transition (EMT) related markers. Luciferase reporter gene assay was employed to inspect the interactions among MEG3, miR-6088, and SMARCB1. Results. MEG3 and SMARCB1 expressions were downregulated in glioma cells. Transfection of pcDNA3.1-MEG3 or pcDNA3.1-SMARCB1 plasmids could clearly block cell proliferation, migration, and EMT progression. MEG3 functions as a sponge for miR-6088, while SMARCB1 is a downstream protein of miR-6088. Transfection of miR-6088 mimic or si-SMARCB1 could obviously reverse the favorable effect of pcDNA3.1-MEG3 on glioma progression. Conclusion. Collectively, the evidence in this study indicated that MEG3 was downregulated in glioma cells and inhibited proliferation and migration of glioma cells via regulating miR-6088/SMARCB1 axis.

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“…LncRNA NEAT1 facilitated oncogene transcription by epigenetic modification of gene promoter in PC-3 and VAaP cells [15]. LncRNA MEG3 sponged miR-9-5p, upregulated QKI-5 and suppressed prostate cancer cell proliferation, migration, invasion and induced apoptosis [16]. Fer-1-like protein 4 (FER1L4) have recently attracted the researchers' attention due to its involvement in the progression of cancer [17,18].…”

Section: Introductionmentioning

confidence: 99%

Long non-coding RNA FER1L4 inhibits prostate cancer progression via sponging miR-92a-3p and upregulation of FBXW7

Huo

Wang

2020

Cancer Cell Int

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Background: Dysregulation of long non-coding RNAs (lncRNAs) is involved in development of prostate cancer. However, the molecular mechanisms of many lncRNAs in prostate cancer have not been studied yet. Methods: The lncRNA Fer-1-like protein 4 (FER1L4) expression was explored in prostate tumors and normal prostate tissues by RT-qPCR and bioinformatic analysis. Overexpression of FER1L4 was performed to evaluate its role in prostate cancer cell proliferation and survival. The molecular mechanism of FER1L4 was investigated by dual luciferase reporter assay, RNA pull down assay, western blotting and RT-qPCR. Results: It was found that FER1L4 was lower in prostate cancer tissues than normal tissues. Higher expression of FER1L4 was associated with prostate cancer tissues of early stage (AJCC stage I/II). Overexpression of FER1L4 inhibited cell proliferation and promoted cell apoptosis in prostate cancer cells. Bioinformatic analysis, RT-qPCR, RNA pull down assay and dual luciferase assay showed that FER1L4 upregulated F-box/WD repeat-containing protein 7 (FBXW7) tumor suppressor via sponging miR-92a-3p. Silencing of FBXW7 reversed the cell phenotypes caused by FER1L4 overexpression in prostate cancer cells. Conclusion: The data demonstrated that FER1L4, a downregulated lncRNA in prostate cancer, was pivotal for cell proliferation and survival of prostate cancer. The study provided new sights into understanding of the signaling network in prostate cancer and implied that FER1L4 might be a biomarker for patients with prostate cancer.

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LncRNA MEG3 inhibits the progression of prostate cancer by modulating miR‐9‐5p/QKI‐5 axis

Cited by 136 publications

References 20 publications

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

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

Tumor-Suppressive Function of lncRNA-MEG3 in Glioma Cells by Regulating miR-6088/SMARCB1 Axis

Long non-coding RNA FER1L4 inhibits prostate cancer progression via sponging miR-92a-3p and upregulation of FBXW7

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