Evidence map›Paper›PMID 24736727›Full record

ArticlePloS one2014

MiR-330-mediated regulation of SH3GL2 expression enhances malignant behaviors of glioblastoma stem cells by activating ERK and PI3K/AKT signaling pathways.

Yilong Yao, Yixue Xue, Jun Ma, Chao Shang, Ping Wang, Libo Liu, Wenjing Liu, Zhen Li, Shengtao Qu, Zhiqing Li and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

29 citing papers in PubMed, 54 citations in OpenAlex.

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  14. Research on human glioma stem cells in China.Neural regeneration research · 2017
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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

11 authors at 2 institutions in 1 country.

Yilong YaoDepartment of Neurosurgery, Shengjing Hospital of China Medical University, Shenyang, Liaoning Province, People's Republic of China.
Yixue XueDepartment of Neurobiology, College of Basic Medicine, China Medical University, Shenyang, Liaoning Province, People's Republic of China; Institute of Pathology and Pathophysiology, China Medical University, Shenyang, Liaoning Province, People's Republic of China.
Jun MaDepartment of Neurobiology, College of Basic Medicine, China Medical University, Shenyang, Liaoning Province, People's Republic of China; Institute of Pathology and Pathophysiology, China Medical University, Shenyang, Liaoning Province, People's Republic of China.
Chao ShangDepartment of Neurobiology, College of Basic Medicine, China Medical University, Shenyang, Liaoning Province, People's Republic of China; Institute of Pathology and Pathophysiology, China Medical University, Shenyang, Liaoning Province, People's Republic of China.
Ping WangDepartment of Neurobiology, College of Basic Medicine, China Medical University, Shenyang, Liaoning Province, People's Republic of China; Institute of Pathology and Pathophysiology, China Medical University, Shenyang, Liaoning Province, People's Republic of China.
Libo LiuDepartment of Neurobiology, College of Basic Medicine, China Medical University, Shenyang, Liaoning Province, People's Republic of China; Institute of Pathology and Pathophysiology, China Medical University, Shenyang, Liaoning Province, People's Republic of China.
Wenjing LiuDepartment of Neurology, The First Affiliated Hospital, China Medical University, Shenyang, Liaoning Province, People's Republic of China.
Zhen LiDepartment of Neurosurgery, Shengjing Hospital of China Medical University, Shenyang, Liaoning Province, People's Republic of China.
Shengtao QuDepartment of Neurosurgery, Shengjing Hospital of China Medical University, Shenyang, Liaoning Province, People's Republic of China.
Zhiqing LiDepartment of Neurobiology, College of Basic Medicine, China Medical University, Shenyang, Liaoning Province, People's Republic of China.
Yunhui LiuDepartment of Neurosurgery, Shengjing Hospital of China Medical University, Shenyang, Liaoning Province, People's Republic of China.
China Medical University · CNFirst Hospital of China Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNAs are currently considered as an active and rapidly evolving area for the treatment of tumors. In this study, we elucidated the biological significance of miR-330 in glioblastoma stem cells (GSCs) as well as the possible molecular mechanisms. SH3GL2 is mainly distributed in the central nervous system and considered to be a tumor suppressor in many tumors. In the present study, we identified miR-330 as a potential regulator of SH3GL2 and we found that it was to be inversely correlated with SH3GL2 expression in GSCs which were isolated from U87 cell lines. The expression of miR-330 enhanced cellular proliferation, promoted cell migration and invasion, and dampened cell apoptosis. When the GSCs were co-transfected with the plasmid containing short hairpin RNA directed against human SH3GL2 gene and miR-330 mimic, we found that miR-330 promoted the malignant behavior of GSCs by down-regulating the expression of SH3GL2. Meanwhile, the ERK and PI3K/AKT signaling pathways were significantly activated, leading to the decreased expression of apoptotic protein and increased expression of anti-apoptotic protein. Furthermore, in orthotopic mouse xenografts, the mice given stable over-expressed SH3GL2 cells co-transfected with miR-330 knockdown plasmid had the smallest tumor sizes and longest survival. In conclusion, these results suggested that miR-330 negatively regulated the expression of SH3GL2 in GSCs, which promoted the oncogenic progression of GSCs through activating ERK and PI3K/AKT signaling pathways. The elucidation of these mechanisms will provide potential therapeutic approaches for human glioblastoma.

Indexed as

Signal TransductionAdaptor Proteins, Signal TransducingAnimalsApoptosisCell Line, TumorCell MovementCell ProliferationDisease Models, AnimalExtracellular Signal-Regulated MAP KinasesGene Expression Regulation, NeoplasticGene Knockdown TechniquesGlioblastomaHumansMiceMicroRNAsNeoplastic Stem CellsAdaptor Proteins, Signal TransducingExtracellular Signal-Regulated MAP KinasesMicroRNAsMIRN330 microRNA, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSH3GL2 protein, human

Identifiers

PMID24736727
PMCPMC3988141
OpenAlexW2039533054

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Registered trials

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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.