Micro<scp>RNA</scp> 152 regulates hepatic glycogenesis by targeting <scp>PTEN</scp>

Wang, Shuyue; Wang, Lilin; Dou, Lin; Guo, Jun; Fang, Weiwei; Li, Meng; Meng, Xiangyu; Man, Yong; Shen, Tao; Huang, Xiuqing; Li, Jian

doi:10.1111/febs.13713

Cited by 34 publications

(26 citation statements)

References 43 publications

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“…This was confirmed in studies on ovarian cancer, breast cancer, pancreatic cancer and prostate cancer [ 13 , 27 – 29 ]. MiR-152-3p, one of the two mature miR-152 sequences, shares the same seed sequence of approximately 6–7 nucleotides with the other members of miR-152 family; the aberrant expression of miR-152-3p was reported to be related to the pathogenesis of tumours such as hepatitis B virus-related hepatocellular carcinoma [ 13 , 30 ]. In the present study, we showed that miR-152-3p directly targeted DNMT1.…”

Section: Discussionmentioning

confidence: 99%

Regulation of human glioma cell apoptosis and invasion by miR-152-3p through targeting DNMT1 and regulating NF2

Sun¹,

Tian²,

Zhang³

et al. 2017

J Exp Clin Cancer Res

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BackgroundMiRNAs are involved in aberrant DNA methylation through regulation of DNA methyltransferases (DNMTs) in the pathogenesis and progression of glioblastomas (GBM). MiR-152-3p was down-expressed in human malignancies, and served as a tumor suppressor. Neurofibromatosis type 2 (NF2) was significantly decreased in GBM tissues with a high level of methylation. However, the link between miR-152-3p, DNMT1 and methylation of NF2 in GBM is not clearly established. This study was conducted to detect the mechanism between miR-152-3p, DNMT1 and NF2 in GBM.MethodsThe levels of DNMT1 and NF2 expression were studied by qRT-PCR, Western blot, immunofluorescence, and immumohistochemical staining. Methylation in the promoter region of NF2 was detected by methylation-specific PCR and bisulfate genomic sequencing PCR. Cell proliferation was examined by Cell-Counting Kit-8 and 5-ethynyl-2′-deoxyuridine assay, and cell invasion was evaluated by transwell assay. Flow cytomery and Hoechst staining were used to analyze cell apoptosis. A dual luciferase system was used to confirm the relationship between miR-152-3p and DNMT1.ResultsMethylation of NF2 and DNMT1 was markedly increased, and miR-152-3p was downregulated in GBM tissues and glioma cells. Both knockdown of DNMT1 and overexpression miR-152-3p showed that demethylation activated the expression of NF2. Furthermore, miR-152-3p directly targeted DNMT1. Both miR-152-3p overexpression and DNMT1 knockdown significantly induced cell apoptosis and inhibited invasive activity. This was also observed after NF2 overexpression.ConclusionsThese results indicated that miR-152-3p can inhibit glioma cell proliferation and invasion activities by decreasing DNMT1. The restoration of miR-152-3p may have therapeutic application in the treatment of GBM.Electronic supplementary materialThe online version of this article (doi:10.1186/s13046-017-0567-4) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

Regulation of human glioma cell apoptosis and invasion by miR-152-3p through targeting DNMT1 and regulating NF2

Sun¹,

Tian²,

Zhang³

et al. 2017

J Exp Clin Cancer Res

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“…High GDNF levels may inhibit P53 expression by up-regulating hsa-miR-183-5p to promote glioma development. In addition, bioinformatics analysis revealed that up-regulated hsa-miR-152-3p targets TP53 and another tumor suppressor, phosphatase and tensin homolog deleted on chromosome ten (PTEN) [69, 70]; it is also involved in glioma cell invasion and angiogenesis via neuropilin 2 (NRP-2) and MMP-3 [71]. Tumor protein p53-inducible nuclear protein 1 (TP53INP1) and apoptosis-stimulating of p53 protein 2 (TP53BP2) are the target genes of hsa-miR-205-5p and participate in the regulation of P53 activity [72, 73].…”

Section: Discussionmentioning

confidence: 99%

MiRNAs Mediate GDNF-Induced Proliferation and Migration of Glioma Cells

Zhang

Dong²,

Guo

et al. 2017

Cell Physiol Biochem

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Background/Aims: Glial cell line-derived neurotrophic factor (GDNF) is an important factor promoting invasive glioma growth. This study was performed to reveal a unique mechanism of glioma cell proliferation and migration. Methods: Human U251 glioma cells were used to screen the optimal GDNF concentration and treatment time to stimulate proliferation and migration. MicroRNA (MiRNA) expression profiles were detected by microarray and confirmed by real-time polymerase chain reaction (PCR). The target genes of differentially expressed miRNAs were predicted by miRWalk, and those targeted by multiple miRNAs were screened with Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses. A regulatory miRNA network was constructed using ingenuity pathway analysis (IPA). Target gene expression of differentially expressed miRNAs was examined by real-time PCR or mRNA microarray. Results: The results show that 50 ng/mL GDNF for 24 h significantly promotes U251 glioma cell proliferation and migration (P < 0.05). Seven miRNAs (hsa-miR-194-5p, hsa-miR-152-3p, hsa-miR-205-5p, hsa-miR-629-5p, hsa-miR-3609, hsa-miR-183-5p, and hsa-miR-487b-3p) were significantly up-regulated after GDNF treatment (P < 0.05). These miRNAs are primarily involved in signal transduction, cell adhesion and cell cycle through mitogen-activated protein kinase (MAPK) signaling, focal adhesion and glioma signal pathways. Five of these miRNAs (hsa-miR-194-5p, hsa-miR-152-3p, hsa-miR-205-5p, hsa-miR-183-5p, and hsa-miR-487b-3p) co-regulate TP53 and Akt. mRNA expression levels of four genes co-targeted by two or more up-regulated miRNAs were significantly decreased after GDNF treatment (P < 0.05). Conclusion: GDNF treatment of U251 glioma cells significantly increased the expression of seven miRNAs involved in cell adhesion and the cell cycle.

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“…miRs are a cluster of small, non-coding RNAs. Numerous miRs have important roles in the regulation of the activation of the insulin signalling pathway, including miR-291b-3p (18), miR-200s (19), miR-152 (20), miR-20a-5p (21), miR-19a (22) and miR-301a (23). The results of our previous study suggested that miR-338-3p regulates the AKT/GSK pathway via targeting of PP4R1, which subsequently regulates protein phosphatase 4 (PP4) expression (11).…”

Section: Discussionmentioning

confidence: 99%

miR‑338‑3p mediates gluconeogenesis via targeting of PP4R1 in hepatocytes

Wang

Chen³

et al. 2018

Mol Med Report

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Hyperglycaemia is a characteristic of type 2 diabetes. In hepatocytes, impaired insulin sensitivity leads to increased gluconeogenesis and decreased glycogenesis. MicroRNA (miR)‑338‑3p is associated with tumour necrosis factor (TNF)‑α‑induced suppression of hepatic glycogenesis via regulation of protein phosphatase 4 regulatory subunit 1 (PP4R1). However, the effect of miR‑338‑3p on gluconeogenesis in hepatocytes remains unknown. In a previous study, it was demonstrated that miR‑338‑3p is downregulated in the livers of mice and in mouse HEPA1‑6 hepatocytes following treatment with TNF‑α. In the present study, the effect of miR‑338‑3p on TNF‑α‑induced gluconeogenesis in hepatocytes was investigated. The levels of phosphorylated‑FOXO1/FOXO1, phosphoenolpyruvate carboxykinase (PEPCK), peroxisome proliferator‑activated receptor γ coactivator (PGC‑1α) and glucose‑6‑phosphatase (G6Pase) were measured by western blotting. The mRNA levels of PEPCK, PGC‑1α and G6Pase were determined by quantitative polymerase chain reaction. Pyruvate tolerance testing was used to determine the gluconeogenesis of mouse livers. The results demonstrated that treatment with TNF‑α resulted in increased levels of gluconeogenesis in the livers of mice and decreased miR‑338‑3p expression levels in HEPA1‑6 cells. Overexpression of miR‑338‑3p reversed TNF‑α‑induced glucose production via enhancement of phosphorylated forkhead box O1 levels and downregulation of the expression levels of genes associated with gluconeogenesis, including peroxisome proliferator‑activated receptor γ coactivator‑1α, phosphoenolpyruvate carboxykinase and glucose‑6‑phosphatase. However, inhibition of miR‑338‑3p expression was revealed to enhance gluconeogenesis in the livers of mice and in HEPA1‑6 cells. Furthermore, downregulation of PP4R1 was revealed to attenuate the effect on glucose production following treatment with miR‑338‑3p inhibitors. In conclusion, the results of the present study revealed that miR‑338‑3p may be involved in TNF‑α‑mediated gluconeogenesis via targeting of PP4R1 in hepatocytes.

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MicroRNA 152 regulates hepatic glycogenesis by targeting PTEN

Cited by 34 publications

References 43 publications

Regulation of human glioma cell apoptosis and invasion by miR-152-3p through targeting DNMT1 and regulating NF2

Regulation of human glioma cell apoptosis and invasion by miR-152-3p through targeting DNMT1 and regulating NF2

MiRNAs Mediate GDNF-Induced Proliferation and Migration of Glioma Cells

miR‑338‑3p mediates gluconeogenesis via targeting of PP4R1 in hepatocytes

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