miRNA-451 inhibits glioma cell proliferation and invasion by downregulating glucose transporter 1

Guo, Hongbao; Yang, Nan; Zhen, Yingwei; Zhang, Yahui; Guo, Lei; Yu, Kai; Huang, Qiang; Zhong, Yue

doi:10.1007/s13277-016-5219-3

Cited by 52 publications

(38 citation statements)

References 43 publications

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“…Differential expression of specific microRNAs (miRNAs or miRs) in gliomas compared with normal tissues has previously been reported (9)(10)(11). miRNAs are single-stranded, highly conserved non-coding RNA molecules (19)(20)(21)(22)(23)(24)(25) nucleotides in length) that regulate the expression of >60% of human genes (12).…”

Section: Introductionmentioning

confidence: 99%

microRNA-188 acts as a tumour suppressor in glioma by directly targeting the IGF2BP2 gene

Guo

2017

Molecular Medicine Reports

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Glioma is the most common and aggressive human brain tumour and accounts for ~35‑61% of intracranial tumours. Despite considerable advances in treatments for glioma, the prognosis for patients with this disease remains unsatisfactory. MicroRNAs (miRNAs of miRs) are small regulatory RNA molecules that have been identified as being involved in the initiation and progression of human cancers, and represent novel therapeutic targets for anticancer treatments. The dysregulation of miR‑188 has been reported in various kinds of human cancer. However, its expression pattern, biological roles and potential mechanism in glioma remain unknown. Expression levels of miR‑188 in glioma tissues and cell lines were detected through reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR). Cell Counting Kit-8 assays and migration and invasion assays were used to explore the effects of miR‑188 on the proliferation, migration and invasion of glioma cells, respectively. Bioinformatics analysis and luciferase reporter assays were performed to examine insulin‑like growth factor 2 mRNA-binding protein 2 (IGF2BP2) as a target gene of miR‑188. RT‑qPCR and Spearman's correlation analysis were then performed to measure IGF2BP2 mRNA expression in clinical glioma tissues and its correlation with miR‑188 expression. The regulatory effect of miR‑188 on IGF2BP2 expression was also investigated through RT‑qPCR and western blotting analysis. Finally, the biological roles of IGF2BP2 in glioma cells were assessed. miR‑188 levels were significantly reduced in glioma tissues and cell lines compared with adjacent normal tissues and normal human astrocytes, respectively. In addition, miR‑188 overexpression suppressed cell proliferation, migration and invasion of glioma. The present study identified IGF2BP2 as a direct target of miR‑188 in glioma, and IGF2BP2 under‑expression served tumour‑suppressive roles in glioma growth and metastasis. Thus, miR‑188 had a similar role in glioma by inhibiting the action of its downstream target, IGF2BP2. Therefore, miR‑188 may be a potential therapeutic target for the prevention and treatment of patients with glioma.

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Section: Introductionmentioning

confidence: 99%

microRNA-188 acts as a tumour suppressor in glioma by directly targeting the IGF2BP2 gene

Guo

2017

Molecular Medicine Reports

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“…Glucose as well as glutamine are important substrates for glycolysis and glutaminolysis, which are important to glioma development and a more aggressive behavior through regulation of the cell cycle at distinct stages (Colombo et al 2011;Yalcin et al 2014;Zhao et al 2017). It has been shown that down-regulation of glucose transporter 1 by microRNA miR-451 inhibits the glucose metabolism and proliferation as well as invasion of glioma cells (Guo et al 2016).…”

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confidence: 99%

Effect of glucose deprivation on the expression of genes encoding glucocorticoid receptor and some related factors in ERN1-knockdown U87 glioma cells

Riabovol

Tsymbal

Minchenko

et al. 2019

Endocrine Regulations

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Objective. The aim of the present study was to examine the effect of glucose deprivation on the expression of genes encoded glucocorticoid receptor (NR3C1) and some related proteins (NR3C2, AHR, NRIP1, NNT, ARHGAP35, SGK1, and SGK3) in U87 glioma cells in response to inhibition of endoplasmic reticulum stress signaling mediated by ERN1/IRE1 (endoplasmic reticulum to nucleus signaling 1/inositol requiring enzyme 1) for evaluation of their possible significance in the control of glioma growth through endoplasmic reticulum stress signaling mediated by IRE1 and glucose deprivation.Methods. The expression of NR3C1, NR3C2, AHR, NRIP1, NNT, ARHGAP35, SGK1, and SGK3 genes in U87 glioma cells transfected by empty vector pcDNA3.1 (control cells) and cells without ERN1 signaling enzyme function (transfected by dnERN1) under glucose deprivation was studied by real time quantitative polymerase chain reaction.Results. It was shown that the expression level of NR3C2, AHR, SGK1, SGK3, and NNT genes was up-regulated in control U87 glioma cells under glucose deprivation condition in comparison with the control cells growing with glucose. At the same time, the expression of NRIP1 gene is down-regulated in these glioma cells under glucose deprivation, but NR3C1 and ARHGAP35 genes was resistant to this experimental condition. We also showed that inhibition of ERN1 signaling enzyme function significantly modified the response of most studied gene expressions to glucose deprivation condition. Thus, effect of glucose deprivation on the expression level of NR3C2, AHR, and SGK1 genes was significantly stronger in ERN1 knockdown U87 glioma cells since the expression of NNT gene was resistant to glucose deprivation condition. Moreover, the inhibition of ERN1 enzymatic activities in U87 glioma cells led to up-regulation of ARHGAP35 gene expression and significant down-regulation of the expression of SGK3 gene in response to glucose deprivation condition.Conclusions. Results of this study demonstrated that glucose deprivation did not change the expression level of NR3C1 gene but it significantly affected the expression of NR3C2, AHR, NRIP, SGK1, SGK3, and NNT genes in vector-transfected U87 glioma cells in gene specific manner and possibly contributed to the control of glioma growth since the expression of most studied genes in glucose deprivation condition was significantly dependent on the functional activity of IRE1 signaling enzyme.

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“…It has been reported that miR-451 was directly involved in the development of drug resistance of several types of cancers, such as non-small-cell lung cancer (NSCLC), colon carcinoma and glioblastoma. 17 , 18 , 19 Although these studies have showed that the potential role of miR-451 in chemoresistance in human cancer, the function of miR-451 in BC remains poorly understood.…”

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Involvement of miR-451 in resistance to paclitaxel by regulating YWHAZ in breast cancer

et al. 2017

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MicroRNAs (miRNAs) have been identified as major post-transcriptional regulators of the initiation and progression of human cancers, including breast cancer. However, the detail role of miR-451 has not been fully elucidated in breast cancer. In this study, we aimed to investigate the biological role and molecular mechanisms of miR-451 in drug resistance in breast cancer cell lines and in xenograft model. We show that miR-451 is decreased in human breast cancer specimens and in paclitaxel-resistant (PR) cells. Ectopic expression of miR-451 could inhibit the cell migration and invasion, promoted apoptosis, induced cell-cycle arrest Furthermore, tyrosine3-monooxygenase/tryptophan5-monooxygenase activation protein zeta (YWHAZ) was identified as a direct target of miR-451. Remarkably, the expression of YWHAZ is inversely correlated with the level of miR-451 in human breast cancer samples. Co-treatment with miR-451 mimics and YWHAZ-siRNA significantly enhanced YWHAZ knockdown in both SKBR3/PR and MCF-7/PR cells Moreover, miR-451 markedly inhibited expression of β-catenin via YWHAZ and subsequently inhibited downstream gene cyclin D1, c-Myc expression. The results of xenograft model in vivo showed that intratumor injection of miR-451 agomir induced a tumor-suppressive effect in SKBR3/PR drug-resistant xenograft model. Taken together, our findings suggested that miR-451 might be considered as important and potential target in paclitaxel-resistant breast cancer treatment.

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miRNA-451 inhibits glioma cell proliferation and invasion by downregulating glucose transporter 1

Cited by 52 publications

References 43 publications

microRNA-188 acts as a tumour suppressor in glioma by directly targeting the IGF2BP2 gene

microRNA-188 acts as a tumour suppressor in glioma by directly targeting the IGF2BP2 gene

Effect of glucose deprivation on the expression of genes encoding glucocorticoid receptor and some related factors in ERN1-knockdown U87 glioma cells

Involvement of miR-451 in resistance to paclitaxel by regulating YWHAZ in breast cancer

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