Lnc<scp>RNA MALAT</scp>1/miR‐129 axis promotes glioma tumorigenesis by targeting <scp>SOX</scp>2

Zhang, Xiong; Wang, Luyang; Wang, Qiangping; Yuan, Ye

doi:10.1111/jcmm.13667

Cited by 66 publications

(54 citation statements)

References 32 publications

(33 reference statements)

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“…MALAT1 has been shown to promote the migration and invasion of lung cancer cells through targeting miR-206 and Akt/mechanistic target of rapamycin (mTOR) signaling (Tang, Xiao, Chen, & Deng, 2018). Also, MALAT1/miR-129 axis promoted glioma tumorigenesis by targeting SOX2 (Xiong, Wang, Wang, & Yuan, 2018). Therefore, sponging miRNA is an important mechanism of MALAT1 in its functions.…”

Section: Discussionmentioning

confidence: 99%

LncRNA MALAT1 protects cardiomyocytes from isoproterenol‐induced apoptosis through sponging miR‐558 to enhance ULK1‐mediated protective autophagy

Guo

Yan

et al. 2018

Journal Cellular Physiology

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Investigating the molecular mechanisms of myocardial infarction (MI) and subsequent heart failure have gained considerable attention worldwide. Long noncoding RNA (lncRNA) metastasis‐associated lung adenocarcinoma transcript 1 (MALAT1) has been previously demonstrated to regulate the proliferation and metastasis of several tumors. However, little is known about the effects of MALAT1 in MI and in regulating the cell date after MI. In our study, first, it was shown that the expression levels of MALAT1 were increased in the MI samples compared with normal tissues using quantitative reverse‐transcription polymerase chain reaction. Then, MALAT1 knockdown could significantly decrease the cell viability and increase the apoptotic rates in isoproterenol (ISO)‐treated H9C2 cells. In addition, we screened the possible target and found that miR‐558 is its direct target using dual luciferase reporter assay, indicating that MALAT1 functioned as decoys sponging miR‐558. Transfection of miR‐558 mimic decreased the cell viability and enhanced the apoptosis. Furthermore, we revealed that miR‐558 could downregulate ULK1 expression and suppressed ISO‐induced protective autophagy. Activation of MALAT1/miR‐558/ULK1 pathway protected H9C2 cells from ISO‐induced mitochondria‐dependent apoptosis. Finally, we used MALAT1‐knockout mice to further demonstrated that MALAT1 protected cardiomyocytes from apoptosis and partially improved the cardiac functions upon ISO treatment. In conclusion, we elucidated that lncRNA MALAT1 protected cardiomyocytes from ISO‐induced apoptosis by sponging miR‐558 thus promoting ULK1‐dependent autophagy. Targeting lncRNA MALAT1 might become a potential strategy in protecting cardiomyocytes during MI.

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Section: Discussionmentioning

confidence: 99%

LncRNA MALAT1 protects cardiomyocytes from isoproterenol‐induced apoptosis through sponging miR‐558 to enhance ULK1‐mediated protective autophagy

Guo

Yan

et al. 2018

Journal Cellular Physiology

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“…After reaching 80% confluence, the GTCs were detached with trypsin and then stained with anti-CD24-FITC and anti-CD44-PE (Invitrogen, Carlsbad, CA, USA) antibodies (10 µg per 10 6 cells). The CD44 + CD24 − cells were considered to be GSCs (10). Microglia cells (HMC3, ATCC R CRL-3304 TM ) were obtained from the American Type Culture Collection (ATCC, VA, USA), which were stimulated with lipopolysaccharide (LPS, 1 µg/ml) and cultured in RPMI-1640 medium (Gibco, Scoresby, VIC, Australia) supplemented with 10% FBS and 1% glutamine.…”

Section: Cell Culturementioning

confidence: 99%

Extracellular Vesicle lncRNA Metastasis-Associated Lung Adenocarcinoma Transcript 1 Released From Glioma Stem Cells Modulates the Inflammatory Response of Microglia After Lipopolysaccharide Stimulation Through Regulating miR-129-5p/High Mobility Group Box-1 Protein Axis

Yang

Sun

et al. 2020

Front. Immunol.

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Glioma stem cell (GSC)-derived extracellular vesicles (EVs) can mediate the communication between GSCs and microglia. Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) expression in GSCs, EVs, and supernatant was detected by real-time PCR. The direct targeting between MALAT1 and miR-129-5p, miR-129-5p, and HMGB1 were tested with luciferase reporter analysis. The expression and secretion of interleukin (IL)-6, IL-8, and tumor necrosis factor (TNF)-α were determined in lipopolysaccharide-stimulated microglia or miR-129-5p inhibitor transferred to microglia exposed to GSC EVs or EVs derived from siMALAT1 pre-transferred GSCs. MALAT1 was enriched in GSC EVs compared with GSCs, and up-regulated MALAT1 was also observed in microglia upon GSC EVs incubation. The relative expression and secretion of IL-6, IL-8, and TNF-α in lipopolysaccharide-stimulated microglia were up-regulated in the GSC supernatant group, which could be reversed by dimethyl amiloride (DMA) (EV secretion inhibitor) co-administration or si-MALAT1 pre-transfection of GSCs. Luciferase reporter assay testified the direct binding of MALAT1 and miR-129-5p, miR-129-5p, and HMGB1, and si-MALAT1 could up-regulate miR-129-5p expression and down-regulate HMGB1 expression in microglia cells. The concentration of IL-6, IL-8, and TNF-α in lipopolysaccharide-stimulated microglia exposed to EVs from siMALAT1 Yang et al. Extracellular Vesicle lncRNA MALAT1 transfected GSCs could be up-regulated by miR-129-5p inhibition. EVs lncRNA MALAT1 released from GSCs could modulate the inflammatory response of microglia after lipopolysaccharide stimulation through regulating the miR-129-5p/HMGB1 axis.

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“…e dysregulation of lncRNAs in glioma has been revealed. For example, lncRNA MALAT1 enhances the activity and proliferation ability of glioma stem cells and promotes glioma tumorigenesis [9]. LncRNA maternally expressed gene 3 (MEG3), located on human chromosome 14q32.3, is a tumor suppressor gene [10].…”

Section: Introductionmentioning

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 MALAT1/miR‐129 axis promotes glioma tumorigenesis by targeting SOX2

Cited by 66 publications

References 32 publications

LncRNA MALAT1 protects cardiomyocytes from isoproterenol‐induced apoptosis through sponging miR‐558 to enhance ULK1‐mediated protective autophagy

LncRNA MALAT1 protects cardiomyocytes from isoproterenol‐induced apoptosis through sponging miR‐558 to enhance ULK1‐mediated protective autophagy

Extracellular Vesicle lncRNA Metastasis-Associated Lung Adenocarcinoma Transcript 1 Released From Glioma Stem Cells Modulates the Inflammatory Response of Microglia After Lipopolysaccharide Stimulation Through Regulating miR-129-5p/High Mobility Group Box-1 Protein Axis

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

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