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

Overview of attention for article published in Journal of Experimental & Clinical Cancer Research, August 2017
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Mentioned by

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3 tweeters

Citations

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56 Dimensions

Readers on

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30 Mendeley
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Title
Regulation of human glioma cell apoptosis and invasion by miR-152-3p through targeting DNMT1 and regulating NF2
Published in
Journal of Experimental & Clinical Cancer Research, August 2017
DOI 10.1186/s13046-017-0567-4
Pubmed ID
Authors

Jin Sun, Xinhua Tian, Junqing Zhang, Yanlin Huang, Xiaoning Lin, Luyue Chen, Shizhong Zhang

Abstract

MiRNAs 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. The 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. Methylation 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. These 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.

Twitter Demographics

The data shown below were collected from the profiles of 3 tweeters who shared this research output. Click here to find out more about how the information was compiled.

Mendeley readers

The data shown below were compiled from readership statistics for 30 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 30 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 5 17%
Other 3 10%
Student > Postgraduate 2 7%
Researcher 2 7%
Student > Bachelor 2 7%
Other 3 10%
Unknown 13 43%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 8 27%
Medicine and Dentistry 7 23%
Agricultural and Biological Sciences 1 3%
Social Sciences 1 3%
Neuroscience 1 3%
Other 0 0%
Unknown 12 40%

Attention Score in Context

This research output has an Altmetric Attention Score of 2. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 16 August 2017.
All research outputs
#6,948,516
of 11,618,931 outputs
Outputs from Journal of Experimental & Clinical Cancer Research
#200
of 633 outputs
Outputs of similar age
#140,102
of 266,238 outputs
Outputs of similar age from Journal of Experimental & Clinical Cancer Research
#4
of 10 outputs
Altmetric has tracked 11,618,931 research outputs across all sources so far. This one is in the 37th percentile – i.e., 37% of other outputs scored the same or lower than it.
So far Altmetric has tracked 633 research outputs from this source. They receive a mean Attention Score of 2.5. This one has gotten more attention than average, scoring higher than 64% of its peers.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 266,238 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 43rd percentile – i.e., 43% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 10 others from the same source and published within six weeks on either side of this one. This one has scored higher than 6 of them.