Evidence map›Paper›PMID 31171769›Full record

ArticleCell death & disease2019

Silencing of microRNA-708 promotes cell growth and epithelial-to-mesenchymal transition by activating the SPHK2/AKT/β-catenin pathway in glioma.

Yan Chen, Xubin Deng, Weiquan Chen, Pengwei Shi, Mei Lian, Hongxiao Wang, Kewan Wang, Dadi Qian, Dong Xiao, Hao Long

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.5field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

24 citing papers in PubMed, 51 citations in OpenAlex.

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  14. METTL3-mediated mOncogene · 2021
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 1 country.

Yan ChenDepartment of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Xubin DengAffiliated Cancer Hospital and Institute of Guangzhou Medical University, Guangzhou, China.
Weiquan Chen
Pengwei ShiDepartment of Emergency, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Mei LianGuangdong Provincial Key Laboratory of Cancer Immunotherapy Research and Guangzhou Key Laboratory of Tumor Immunology Research, Cancer Research Institute, Southern Medical University, Guangzhou, China.
Hongxiao WangDepartment of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Kewan WangDepartment of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Dadi QianDepartment of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Dong XiaoGuangdong Provincial Key Laboratory of Cancer Immunotherapy Research and Guangzhou Key Laboratory of Tumor Immunology Research, Cancer Research Institute, Southern Medical University, Guangzhou, China. Xiao_d@hotmail.com.
Hao LongDepartment of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, China. longh812@163.com.
Nanfang Hospital · CNSouthern Medical University · CNGuangzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aberrant microRNA-708 (miR-708) expression is frequently reported in cancer studies; however, its role in glioma has not been examined in detail. We investigated miR-708 function in glioma and revealed that miR-708 expression was significantly down-regulated in glioma tissues and cell lines. Restoration of miR-708 inhibited glioma cell growth and invasion both in vitro and in vivo. The oncogene SPHK2 (sphingosine kinase 2) was identified as a downstream target of miR-708 using luciferase and western blot assays. miR-708 inhibited AKT/β-catenin signaling, which is activated by SPHK2. In addition, we revealed that miR-708 was transcriptionally repressed by EZH2 (enhancer of zeste homolog 2)-induced histone H3 lysine 27 trimethylation and promoter methylation. In summary, our findings revealed that miR-708 is a glioma tumor suppressor and suggest that miR-708 is a potential therapeutic target for glioma patients.

Indexed as

Animalsbeta CateninBrain NeoplasmsCell CycleCell Line, TumorCell ProliferationDown-RegulationEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticGliomaGlycogen Synthase KinasesHistonesHumansMethylationMiceMice, Nudebeta CateninCTNNB1 protein, humanGlycogen Synthase KinasesHistonesMicroRNAsMIRN708 microRNA, humanPhosphotransferases (Alcohol Group Acceptor)Proto-Oncogene Proteins c-aktSphingosine Kinasesphingosine kinase 2, human

Identifiers

PMID31171769
PMCPMC6554356
OpenAlexW2948985166

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.