Hsa-let-7c-5p augments enterovirus 71 replication through viral subversion of cell signaling in rhabdomyosarcoma cells

Zhou, Benhong; Chu, Min; Xu, Shanshan; Chen, Xiong; Liu, Yongjuan; Wang, Wenwen; Zhang, Fengfeng; Han, Song; Yin, Jun; Peng, Biwen; He, Xiaohua; Liu, Wanhong

doi:10.1186/s13578-017-0135-9

Cited by 17 publications

(13 citation statements)

References 59 publications

(47 reference statements)

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“…MAP4K4 contains a let - 7 target site in its 3′-UTR, indicating that let-7 family can regulate MAPK pathways by altering MAP4K4 expression levels 39 , 40 . Hsa-let-7c-5p can facilitate human enterovirus 71 replication by inhibiting MAP4K4 expression; this mechanism might explain the virus’s ability to subvert the JNK pathway 41 . Previous studies have demonstrated that ERK1/2 MAPK negatively regulates let-7 by inducing LIN28 expression through Myc transcription 42 .…”

Section: Discussionmentioning

confidence: 99%

Hsa-let-7c controls the committed differentiation of IGF-1-treated mesenchymal stem cells derived from dental pulps by targeting IGF-1R via the MAPK pathways

Liu

et al. 2018

Exp Mol Med

102

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The putative tumor suppressor microRNA let-7c is extensively associated with the biological properties of cancer cells. However, the potential involvement of let-7c in the differentiation of mesenchymal stem cells has not been fully explored. In this study, we investigated the influence of hsa-let-7c (let-7c) on the proliferation and differentiation of human dental pulp-derived mesenchymal stem cells (DPMSCs) treated with insulin-like growth factor 1 (IGF-1) via flow cytometry, CCK-8 assays, alizarin red staining, real-time RT-PCR, and western blotting. In general, the proliferative capabilities and cell viability of DPMSCs were not significantly affected by the overexpression or deletion of let-7c. However, overexpression of let-7c significantly inhibited the expression of IGF-1 receptor (IGF-1R) and downregulated the osteo/odontogenic differentiation of DPMSCs, as indicated by decreased levels of several osteo/odontogenic markers (osteocalcin, osterix, runt-related transcription factor 2, dentin sialophosphoprotein, dentin sialoprotein, alkaline phosphatase, type 1 collagen, and dentin matrix protein 1) in IGF-1-treated DPMSCs. Inversely, deletion of let-7c resulted in increased IGF-1R levels and enhanced osteo/odontogenic differentiation. Furthermore, the ERK, JNK, and P38 MAPK pathways were significantly inhibited following the overexpression of let-7c in DPMSCs. Deletion of let-7c promoted the activation of the JNK and P38 MAPK pathways. Our cumulative findings indicate that Let-7c can inhibit the osteo/odontogenic differentiation of IGF-1-treated DPMSCs by targeting IGF-1R via the JNK/P38 MAPK signaling pathways.

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Section: Discussionmentioning

confidence: 99%

Hsa-let-7c controls the committed differentiation of IGF-1-treated mesenchymal stem cells derived from dental pulps by targeting IGF-1R via the MAPK pathways

Liu

et al. 2018

Exp Mol Med

102

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“…qRT-PCR was performed with SYBR Green Real-Time PCR Master Mix (Toyobo, Osaka, Japan) according to the manufacturer’s instructions. The qRT-PCR conditions for measuring mRNA levels in cerebellum tissues used in our laboratory have been reported previously [ 58 ]. The primers were as follows: occludin…”

Section: Methodsmentioning

confidence: 99%

Kv1.3 channel blocker (ImKTx88) maintains blood–brain barrier in experimental autoimmune encephalomyelitis

et al. 2017

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BackgroundDisruption of blood–brain barrier (BBB) and subsequent infiltration of auto-reactive T lymphocytes are major characteristics of multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE). Kv1.3 channel blockers are demonstrated potential therapeutic effects on MS patients and EAE models, maybe via reducing activation of T cells. However, it remains to be explored whether Kv1.3 channel blockers maintain integrity of BBB in MS model.ResultsIn this study, ImKTx88, a highly selective Kv1.3 channel blocker, was used to determine the role of Kv1.3 channel in the pathogenesis of EAE, particularly in the maintenance of BBB. ImKTx88 ameliorated pathological severity in the EAE rats, and reduced extravasation into CNS. ImKTx88 also ameliorated the severity of loss or redistribution of tight junction proteins, and inhibited over-expression of ICAM-1 and VCAM-1 in the brain from EAE rats. Furthermore ImKTx88 protection was associated with activation of Ang-1/Tie-2 axis, and might be due to decreased IL-17 production.ConclusionsImKTx88 may be a novel therapeutic agent for MS treatment by stabilizing the BBB.Electronic supplementary materialThe online version of this article (doi:10.1186/s13578-017-0158-2) contains supplementary material, which is available to authorized users.

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“…hsa-miR-181b and hsa-miR-181d were found to be differentially expressed between invasive and non-invasive non-functional pituitary adenoma [ 61 ]. Finally, hsa-let-7c-5p facilitated enterovirus 71 replication through viral subversion of cell signaling in rhabdomyosarcoma cells [ 62 ].…”

Section: Resultsmentioning

confidence: 99%

Random walks on mutual microRNA-target gene interaction network improve the prediction of disease-associated microRNAs

Verbeke

Sơn

et al. 2017

BMC Bioinformatics

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BackgroundMicroRNAs (miRNAs) have been shown to play an important role in pathological initiation, progression and maintenance. Because identification in the laboratory of disease-related miRNAs is not straightforward, numerous network-based methods have been developed to predict novel miRNAs in silico. Homogeneous networks (in which every node is a miRNA) based on the targets shared between miRNAs have been widely used to predict their role in disease phenotypes. Although such homogeneous networks can predict potential disease-associated miRNAs, they do not consider the roles of the target genes of the miRNAs. Here, we introduce a novel method based on a heterogeneous network that not only considers miRNAs but also the corresponding target genes in the network model.ResultsInstead of constructing homogeneous miRNA networks, we built heterogeneous miRNA networks consisting of both miRNAs and their target genes, using databases of known miRNA-target gene interactions. In addition, as recent studies demonstrated reciprocal regulatory relations between miRNAs and their target genes, we considered these heterogeneous miRNA networks to be undirected, assuming mutual miRNA-target interactions. Next, we introduced a novel method (RWRMTN) operating on these mutual heterogeneous miRNA networks to rank candidate disease-related miRNAs using a random walk with restart (RWR) based algorithm. Using both known disease-associated miRNAs and their target genes as seed nodes, the method can identify additional miRNAs involved in the disease phenotype. Experiments indicated that RWRMTN outperformed two existing state-of-the-art methods: RWRMDA, a network-based method that also uses a RWR on homogeneous (rather than heterogeneous) miRNA networks, and RLSMDA, a machine learning-based method. Interestingly, we could relate this performance gain to the emergence of “disease modules” in the heterogeneous miRNA networks used as input for the algorithm. Moreover, we could demonstrate that RWRMTN is stable, performing well when using both experimentally validated and predicted miRNA-target gene interaction data for network construction. Finally, using RWRMTN, we identified 76 novel miRNAs associated with 23 disease phenotypes which were present in a recent database of known disease-miRNA associations.ConclusionsSummarizing, using random walks on mutual miRNA-target networks improves the prediction of novel disease-associated miRNAs because of the existence of “disease modules” in these networks.Electronic supplementary materialThe online version of this article (10.1186/s12859-017-1924-1) contains supplementary material, which is available to authorized users.

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Hsa-let-7c-5p augments enterovirus 71 replication through viral subversion of cell signaling in rhabdomyosarcoma cells

Cited by 17 publications

References 59 publications

Hsa-let-7c controls the committed differentiation of IGF-1-treated mesenchymal stem cells derived from dental pulps by targeting IGF-1R via the MAPK pathways

Hsa-let-7c controls the committed differentiation of IGF-1-treated mesenchymal stem cells derived from dental pulps by targeting IGF-1R via the MAPK pathways

Kv1.3 channel blocker (ImKTx88) maintains blood–brain barrier in experimental autoimmune encephalomyelitis

Random walks on mutual microRNA-target gene interaction network improve the prediction of disease-associated microRNAs

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