miR‑490‑3p functions as a tumor suppressor in glioma by inhibiting high‑mobility group AT‑hook 2 expression

Zhang, Fang; Wu, Anhao; Wang, Yinhui; Liu, Jianmin

doi:10.3892/etm.2019.7606

Cited by 16 publications

(15 citation statements)

References 29 publications

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“…For example, hsa-miR-338-3p found to be significantly downregulated in GBM, acted as a tumorsuppressing gene whose silencing can inhibit malignant biological behaviors of glioma cells, was an independent prognostic biomarker associated with poor prognosis in glioma patients; 28 hsa-miR-139-5p is lower in blood and brain tissues of GBM, was identified as a tumor suppressor by negatively targeting Notch1; 29 hsa-miR-490-3p expression was significantly downregulated in GBM, which can inhibit glioma cell proliferation and migration. 30 GO and KEGG pathway analysis offered insight into the possible roles of DE-miRNAs in the pathogenesis of GBM. We found that the IFN-gamma pathway was involved in the most significantly enriched terms shared by all sample types, indicates that DE-miRNAs in GBM may affect the activation of immune system and is a key factor affecting disease progression.…”

Section: Discussionmentioning

confidence: 99%

<p>Reduced Expression of hsa-miR-338-3p Contributes to the Development of Glioma Cells by Targeting Mitochondrial 3-Oxoacyl-ACP Synthase (OXSM) in Glioblastoma (GBM)</p>

Wang¹,

Lu²

2020

OTT

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Background: MicroRNAs have been identified as major regulators and therapeutic targets of glioblastoma (GBM). It is thus meaningful to study the miRNAs differentially expressed (DE-miRNAs) in GBM. Materials and Methods: We performed a meta-analysis of previously published microarray data using the R-based "metaMA" package to identify DE-miRNAs.The biological processes of the DE-miRNAs were then analyzed using FunRich. KEGG pathways of the DE-miRNAs gene targets were analyzed by mirPath V.3. Luciferase activity assay was performed to validate that OXSM is a direct target of hsa-miR338-3p. Flow cytometry was used to detect the effects of miR-338-3p on GBM cell proliferation, apoptosis and cell cycle. Results: DE-miRNAs in blood and brain tissue from GBM were identified. "Type I interferon signaling pathway" and "VEGF and VEGFR signaling network" were the most significantly enriched biological processes shared by all GBM types. In KEGG pathway analysis, DE-miRNAs both in blood and tissue show altered fatty acid biosynthesis. Further validation shows hsa-miR-338-3p regulates fatty acid metabolism by directly targeting OXSM gene. In addition, our data revealed an accelerated cell cycle and an anti-apoptotic role for OXSM in glioma cells, which has not been reported. Finally, we confirmed that hsa-miR-338-3p inhibitor antagonized the effect of downregulation of OXSM on cell cycle and apoptosis of GBM cells. Conclusion: We revealed that hsa-miR-338-3p, down-regulated in GBM, may affect the biogenesis and rapid proliferation of glioma cells by regulating the level of OXSM, providing new insights into understanding the pathogenesis of GBM and developing strategies to improve GBM prognosis.

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Section: Discussionmentioning

confidence: 99%

<p>Reduced Expression of hsa-miR-338-3p Contributes to the Development of Glioma Cells by Targeting Mitochondrial 3-Oxoacyl-ACP Synthase (OXSM) in Glioblastoma (GBM)</p>

Wang¹,

Lu²

2020

OTT

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“…Igf2bp2 is a target of HMGA2 in different cell types [56,74,75]; it is an mRNA binding protein also involved in stem cell maintenance in glioblastoma [121], a neural tumor in which HMGA2 is reactivated [122][123][124][125]. Similar to Hmga2, Igf2bp2 is initially expressed at high levels in cortical NPCs in the early neurogenic phase, and then downregulated in late NPCs in the gliogenic phase.…”

Section: Hmga1 and Hmga2 In The Development Of The Cnsmentioning

confidence: 99%

HMGA Genes and Proteins in Development and Evolution

Vignali

Marracci

2020

IJMS

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HMGA (high mobility group A) (HMGA1 and HMGA2) are small non-histone proteins that can bind DNA and modify chromatin state, thus modulating the accessibility of regulatory factors to the DNA and contributing to the overall panorama of gene expression tuning. In general, they are abundantly expressed during embryogenesis, but are downregulated in the adult differentiated tissues. In the present review, we summarize some aspects of their role during development, also dealing with relevant studies that have shed light on their functioning in cell biology and with emerging possible involvement of HMGA1 and HMGA2 in evolutionary biology.

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“…The χ 2 test was used to identify the differences in clinicopathological characteristics between the two groups. The results demonstrated that miR-769-3p levels in the serum and glioma tissues were significantly associated with the World Health Organization (WHO) grade (P<0.01) (17) and Karnofsky performance score (KPS; P<0.05) (18). No similar results were observed for other clinicopathological parameters, including age, sex and tumor size (all P>0.05; Table I).…”

Section: Resultsmentioning

confidence: 99%

MicroRNA‑769‑3p inhibits tumor progression in glioma by suppressing ZEB2 and inhibiting the Wnt/β‑catenin signaling pathway

Wang¹,

Yang

Gao³

et al. 2019

Oncol Lett

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Accumulating evidence suggests the crucial role of microRNAs (miRNAs) in human cancers. The present study aimed to investigate the clinical and functional roles of miR-769-3p in glioma, as well as the underlying molecular mechanisms. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to determine the expression levels of miR-769-3p in glioma tissues and cells. Receiver operating characteristic (ROC) curve analysis was applied to calculate the diagnostic value of miR-769-3p. The 5-year survival rate of patients was calculated using Kaplan-Meier analysis and Cox regression analysis. Cell experiments were used to investigate the functional role of miR-769-3p in glioma. The gene target of miR-769-3p was predicted by TargetScan. Changes in the levels of Wnt signaling-related proteins were measured by western blotting. miR-769-3p was significantly downregulated in glioma tissues and serum, as well as in glioma cell lines (P<0.001). miR-769-3p expression was significantly associated with the World Health Organization grade and Karnofsky performance score. The ROC curves demonstrated that serum miR-769-3p level reliably distinguished patients with glioma from healthy individuals. High tissue miR-769-3p expression predicted poor overall survival in patients with glioma (log-rank P=0.001) and was identified as an independent prognostic factor. In addition, zinc finger E-box binding homeobox 2 (ZEB2) was demonstrated to be a direct target of miR-769-3p in glioma cells using a luciferase assay. miR-769-3p upregulation suppressed the activity of the Wnt/β-catenin signaling pathway in glioma cells. In conclusion, miR-769-3p may serve as a diagnostic and prognostic biomarker in patients with glioma and target ZEB2 to inhibit tumor progression via the Wnt/β-catenin signaling pathway. miR-769-3p may be a novel therapeutic target for the treatment of glioma.

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miR‑490‑3p functions as a tumor suppressor in glioma by inhibiting high‑mobility group AT‑hook 2 expression

Cited by 16 publications

References 29 publications

<p>Reduced Expression of hsa-miR-338-3p Contributes to the Development of Glioma Cells by Targeting Mitochondrial 3-Oxoacyl-ACP Synthase (OXSM) in Glioblastoma (GBM)</p>

<p>Reduced Expression of hsa-miR-338-3p Contributes to the Development of Glioma Cells by Targeting Mitochondrial 3-Oxoacyl-ACP Synthase (OXSM) in Glioblastoma (GBM)</p>

HMGA Genes and Proteins in Development and Evolution

MicroRNA‑769‑3p inhibits tumor progression in glioma by suppressing ZEB2 and inhibiting the Wnt/β‑catenin signaling pathway

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