miR-181 subunits enhance the chemosensitivity of temozolomide by Rap1B-mediated cytoskeleton remodeling in glioblastoma cells

She, Xiaoling; Yu, Zhibin; Cui, Yulong; Lei, Qinghua; Wang, Zeyou; Xu, Gang; Luo, Zhaohui; Li, Guiyuan; Wu, Minghua

doi:10.1007/s12032-014-0892-9

Cited by 45 publications

(37 citation statements)

References 36 publications

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“…83 It is generally recognized that miR-21 is upregulated in mouse and human GBM, which is corroborated from The Cancer Genome Atlas. 78 Notably, miR-21 has also been shown to regulate GBM chemotherapeutic resistance, invasion, and apoptosis.…”

Section: Regulating Mir-21 and Pdcd4 For Chemoresistance In Gbmmentioning

confidence: 74%

Targeting strategies on miRNA-21 and PDCD4 for glioblastoma

Wang

Tang

et al. 2015

Archives of Biochemistry and Biophysics

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Section: Regulating Mir-21 and Pdcd4 For Chemoresistance In Gbmmentioning

confidence: 74%

Targeting strategies on miRNA-21 and PDCD4 for glioblastoma

Wang

Tang

et al. 2015

Archives of Biochemistry and Biophysics

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“…They established that miR181a functioned not only as a tumor suppressor, but also played a role as a growth inhibitor, apoptosis inducer, and inhibitor of the invasion of adjacent glioma cells. The down-regulation of miR-181a may be a relevant factor contributing to malignancy in human gliomas (She et al, 2014). Ouyang et al (2012) manipulated the levels of miR-181a in astrocyte cultures by using inhibitors and mimics.…”

Section: Discussionmentioning

confidence: 99%

Silencing miR-181a produces neuroprotection against hippocampus neuron cell apoptosis post-status epilepticus in a rat model and in children with temporal lobe epilepsy

Ren

Zhu

2016

Genet. Mol. Res.

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ABSTRACT. Epilepsy is one of the most frequent neurological disorders. Recently, the regulation of microRNAs was found to be associated with epilepsy, but the molecular mechanism by which microRNA influences epilepsy process remains to be unveiled and the development of microRNA-based therapy requires more intensive research. In this study, five microRNAs with potential relevance to epilepsy were initially chosen: miR-132, miR-146a, miR-181a, miR-34a, and miR-124. Twenty-five children who were patients with epilepsy were selected as subjects to obtain tissue samples for the study. The miRNA-181a, which represented the most increased fold-changes in clinical samples, were then selected for further function study in mouse model. The temporal lobe epilepsy (TLE) model, along with lithium-pilocarpine-induced status epilepticus (SE), was established in Sprague-Dawley rats. The antagomir of miR-181a was used to determine the role of miR-181a in cell apoptosis. Analyses were conducted to determine the expression levels of miR-181a, neuronal apoptosis in post-SE, and activated caspase-3. We found evidence of significant time dependent up-regulation of miR-181a amongst post-SE rats and TLE on 24 h (4.47 ± 0.35), 7 days (4.85 ± 0.53), and 2 weeks (5.66 ± 0.64). Experiments with the miR-181a antagomir showed that this particular miRNA led to the inhibition of the protein expression of caspase-3, and was up-regulated in the course of seizure-induced neuronal apoptosis. This study provided evidence that targeting miR-181a leads to a neuroprotective response and is linked to an increase in the activation of the caspase-3 protein. These findings suggest that miR-181a may serve as a promising therapeutic target for epilepsy.

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“…They are aberrantly expressed in many cancers and can exert tumor suppressive or oncogenic functions [5]. Aberrant expression of miRNAs in glioblastoma has also been reported, and many miRNAs have been shown to participate in glioblastoma tumorigenesis and/or invasion by targeting oncogenes or tumor suppressor genes, including miR-96, miR-101, MiR-125a-5p, miR-128, miR-182, miR-185, and miR-381 [6][7][8][9][10][11][12][13][14][15]. These findings indicate that miRNAs may act as another kind of important regulator in glioblastoma tumorigenesis, in addition to the protein-coding genes.…”

Section: Introductionmentioning

confidence: 99%

miR-25 promotes glioblastoma cell proliferation and invasion by directly targeting NEFL

Peng

Yuan

et al. 2015

Mol Cell Biochem

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Glioblastoma multiforme (GBM) is the most malignant and common brain tumor; it is aggressive growth pattern means that GBM patients face a poor prognosis even when receiving the best available treatment modalities. In recent years, an increasing number of reports suggest that the discovery of microRNAs (miRNAs) might provide a novel therapeutic target for human cancers, including GBM. One miRNA in particular, microRNA-25 (miR-25), is overexpressed in several cancers, wherein accumulating evidence indicates that it functions as an oncogene. However, the function of miR-25 in GBM has not been totally elucidated. In this study, we demonstrated that miR-25 was significantly up-regulated in astrocytoma tissues and glioblastoma cell lines. In vitro studies further demonstrated that overexpressed miR-25 was able to promote, while its antisense oligos inhibited cell proliferation and invasion in U251 cells. Moreover, we identified neurofilament light polypeptide (NEFL) as a novel target molecule of miR-25. Also of note was the fact that NEFL was down-regulated with increased levels of miR-25 expression in human astrocytoma clinical specimens. In addition, via the mTOR signaling pathway, NEFL-siRNA could significantly attenuate the inhibitory effects of knockdown miR-25 on the proliferation and invasion of U251 cells. Overall, our results showed an important role for miR-25 in regulating NEFL expression in GBM, and suggest that miR-25 could be a potential target for GBM treatment.

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miR-181 subunits enhance the chemosensitivity of temozolomide by Rap1B-mediated cytoskeleton remodeling in glioblastoma cells

Cited by 45 publications

References 36 publications

Targeting strategies on miRNA-21 and PDCD4 for glioblastoma

Targeting strategies on miRNA-21 and PDCD4 for glioblastoma

Silencing miR-181a produces neuroprotection against hippocampus neuron cell apoptosis post-status epilepticus in a rat model and in children with temporal lobe epilepsy

miR-25 promotes glioblastoma cell proliferation and invasion by directly targeting NEFL

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