MiRNA-451 Inhibits Glioma Cell Proliferation and Invasion Through the mTOR/HIF-1α/VEGF Signaling Pathway by Targeting CAB39

Yang, Nan; Guo, Hongbao; Guo, Lei; Wang, Le; Ren, Biao; Yu, Kai; Huang, Qiang; Zhong, Yue

doi:10.1089/humc.2018.133

Cited by 63 publications

(45 citation statements)

References 34 publications

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“…Interactions between different cell types occurring in-vivo could also explain the differences noted in the expression of the Ang proteins and their receptor Tie2. miR-451 has been shown to inhibit angiogenesis through targeting MIF, calcium-binding protein 39 (CAB39) and IL-6R mediated pathways that influence expression of VEGF-A [16,35,48]. In our study, administration of a miR-451 inhibitor was also associated with increased expression of VEGF-A.…”

Section: Discussionmentioning

confidence: 52%

“…Normal alveolar development has been shown to be dependent on angiogenesis [4,32,33] and dysregulated vascular growth is a well-established feature of the BPD phenotype [1,4]. miR-451 is a miRNA that has been shown to inhibit the expression of pro-angiogenic and antiapoptotic mediators such as MIF, IL-6R and YWHAZ in a variety of different malignant cell types and tumors [14,16,18,34,35]. In tumors, reduced expression of miR-451 and increased expression of MIF is associated with increased likelihood of progression [15,36]; however, in preterm infants, increased expression of MIF is linked to a reduced risk for BPD [10,11].…”

Section: Discussionmentioning

confidence: 99%

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Inhibition of microRNA-451 is associated with increased expression of Macrophage Migration Inhibitory Factor and mitigation of the cardio-pulmonary phenotype in a murine model of Bronchopulmonary Dysplasia

et al. 2020

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Background: Macrophage migration inhibitory factor (MIF) has been implicated as a protective factor in the development of bronchopulmonary dysplasia (BPD) and is known to be regulated by . The aim of this study was to evaluate the role of miR-451 and the MIF signaling pathway in in vitro and in vivo models of BPD. Methods: Studies were conducted in mouse lung endothelial cells (MLECs) exposed to hyperoxia and in a newborn mouse model of hyperoxia-induced BPD. Lung and cardiac morphometry as well as vascular markers were evaluated. Results: Increased expression of miR-451 was noted in MLECs exposed to hyperoxia and in lungs of BPD mice. Administration of a miR-451 inhibitor to MLECs exposed to hyperoxia was associated with increased expression of MIF and decreased expression of angiopoietin (Ang) 2. Treatment with the miR-451 inhibitor was associated with improved lung morphometry indices, significant reduction in right ventricular hypertrophy, decreased mean arterial wall thickness and improvement in vascular density in BPD mice. Western blot analysis demonstrated preservation of MIF expression in BPD animals treated with a miR-451 inhibitor and increased expression of vascular endothelial growth factor-A (VEGF-A), Ang1, Ang2 and the Ang receptor, Tie2. Conclusion: We demonstrated that inhibition of miR-451 is associated with mitigation of the cardio-pulmonary phenotype, preservation of MIF expression and increased expression of several vascular growth factors.

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Section: Discussionmentioning

confidence: 52%

Section: Discussionmentioning

confidence: 99%

Inhibition of microRNA-451 is associated with increased expression of Macrophage Migration Inhibitory Factor and mitigation of the cardio-pulmonary phenotype in a murine model of Bronchopulmonary Dysplasia

et al. 2020

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“…Among which, miR-451 is a frequently investigated miRNA in glioma. According to several research groups, miR-451 expression is repressed in glioma tissues and cells [18,19]. Besides, miR-451 acted as a tentative switch in mediating glioma cells growth and migration [20][21][22].…”

Section: Introductionmentioning

confidence: 99%

Knockdown of lncRNA LSINCT5 suppresses growth and metastasis of human glioma cells via up-regulating miR-451

Liu

Cao

2019

Artificial Cells, Nanomedicine, and Biotechnology

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Background: Glioma is a main cause of brain-cancer relevant death. The present paper designed to reveal the possible role of LSINCT5 in human glioma GL15 cells. Methods: LSINCT5 and miR-451 expression in glioma tissues was examined using qRT-PCR. The impacts of LSINCT5, miR-451 and Rac1 in GL15 cells were checked by carrying out CCK-8 assay, transwell assay, and flow cytometric analysis. Further, the target gene of LSINCT5 and miR-451 was explored. Accumulation of PI3K/AKT, Wnt/b-catenin and NF-jB pathway proteins was examined using Western blot. Results: LSINCT5 was highly expressed while miR-451 low expressed in glioma tissues when compared to normal controls. Down-regulating LSINCT5 effectively declined GL15 cells viability, migration and invasion, but accelerated apoptosis. Nonetheless, the above-mentioned effects of LSINCT5 down-regulation were weakened when miR-451 was silenced. Rac1 was a target of miR-451. The tumour-suppressive effects of miR-451 on GL15 cells were weakened when Rac1 was overexpressed. Further, LSINCT5-miR-451-Rac1 axis could impact the activation of PI3K/AKT, Wnt/b-catenin and NF-jB pathways. Conclusion: Down-regulation of LSINCT5 represses glioma cells growth and metastasis in vitro likely through targeting miR-451 and thereby inhibiting Rac1-regulated PI3K/AKT, Wnt/b-catenin and NF-jB pathways.

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“…30 MiR-451 suppressed glioma cell proliferation and invasion by blocking the mTOR/HIF-1α/VEGF pathway through regulating CAB39 expression. 31 Propofol has also been found to exert anti-tumor functions via regulating miRNAs in many types of tumors. For instance, Yu et al found propofol promoted cell apoptosis in breast cancer via downregulating miR-24.…”

Section: Discussionmentioning

confidence: 99%

<p>Propofol Inhibits the Migration and Invasion of Glioma Cells by Blocking the PI3K/AKT Pathway Through miR-206/ROCK1 Axis</p>

Wang¹,

Yang²,

Liu³

et al. 2020

OTT

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Background: Propofol has been identified to perform anti-tumor functions in glioma. However, the molecular mechanisms underlying propofol-induced prevention on migration and invasion of glioma cells remain unclear. Methods: Cell proliferation, invasion and migration were measured by 3-(4,5)-dimethylthiahiazo (−z-y1)-3,5-di-phenytetrazoliumromide assay and transwell assay, respectively. The expression of microRNA (miR)-206 and Rho-associated coiled coil-containing protein kinase 1 (ROCK1) was detected by quantitative real-time polymerase chain reaction. Western blot was used to measure the activation of the PI3K/AKT pathway. The interaction between miR-206 and ROCK1 was analyzed using the dual-luciferase reporter assay, RNA immunoprecipitation assay, and pull-down assay. Results: Propofol treatment inhibited the migration, invasion, and PI3K/AKT pathway activation in glioma cells. MiR-206 was decreased in glioma tissues and cells, while propofol exposure induced the upregulation of miR-206 in glioma cells. Besides that, we also found overexpressed miR-206 enhanced propofol-mediated inhibition on the migration, invasion, and PI3K/AKT pathway activation of glioma cells. Subsequently, ROCK1 was confirmed to be a target of miR-206. ROCK1 was elevated in glioma tissues and cells, but was reduced by propofol exposure in glioma cells. The rescue assay indicated that the miR-206/ROCK1 axis was involved in propofol-induced inhibition on the migration, invasion, and PI3K/AKT pathway activation in glioma cells. Conclusion: Propofol inhibited the migration and invasion of glioma cells by blocking the PI3K/AKT pathway through the miR-206/ROCK1 axis, suggesting an effective clinical implication for the anesthetic to prevent the metastasis of glioma.

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MiRNA-451 Inhibits Glioma Cell Proliferation and Invasion Through the mTOR/HIF-1α/VEGF Signaling Pathway by Targeting CAB39

Cited by 63 publications

References 34 publications

Inhibition of microRNA-451 is associated with increased expression of Macrophage Migration Inhibitory Factor and mitigation of the cardio-pulmonary phenotype in a murine model of Bronchopulmonary Dysplasia

Inhibition of microRNA-451 is associated with increased expression of Macrophage Migration Inhibitory Factor and mitigation of the cardio-pulmonary phenotype in a murine model of Bronchopulmonary Dysplasia

Knockdown of lncRNA LSINCT5 suppresses growth and metastasis of human glioma cells via up-regulating miR-451

<p>Propofol Inhibits the Migration and Invasion of Glioma Cells by Blocking the PI3K/AKT Pathway Through miR-206/ROCK1 Axis</p>

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