Evidence map›Paper›PMID 28440461›Full record

ArticleInternational journal of oncology2017

The role of miR-451 in the switching between proliferation and migration in malignant glioma cells: AMPK signaling, mTOR modulation and Rac1 activation required.

Kai Zhao, Leilei Wang, Tao Li, Meng Zhu, Chen Zhang, Lei Chen, Pengfei Zhao, Hua Zhou, Shengping Yu, Xuejun Yang

Open access · hybridAbstract read
In one paragraph

Article in International journal of oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

34 citing papers in PubMed, 47 citations in OpenAlex.

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  9. 3D-ASC-Exos as a novel drug carrier for glioma treatment.Frontiers in cell and developmental biology · 2025
    Article
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  16. miR-451 suppresses EMT and metastasis in glioma cells.Cell cycle (Georgetown, Tex.) · 2021
    Article
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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.

Kai ZhaoDepartment of Neurosurgery, Tianjin Medical University General Hospital, Tianjin 300052, P.R. China.
Leilei WangDepartment of Neurosurgery, Cangzhou Central Hospital, Cangzhou, Hebei 061001, P.R. China.
Tao LiDepartment of Neurosurgery, Tianjin Medical University General Hospital, Tianjin 300052, P.R. China.
Meng ZhuDepartment of Neurosurgery, The Affiliated Hospital of Qingdao University, Qingdao, Shandong 266003, P.R. China.
Chen ZhangDepartment of Neurosurgery, Tianjin Medical University General Hospital, Tianjin 300052, P.R. China.
Lei ChenDepartment of Neurosurgery, Tianjin Medical University General Hospital, Tianjin 300052, P.R. China.
Pengfei ZhaoDepartment of Neurosurgery, Tianjin Medical University General Hospital, Tianjin 300052, P.R. China.
Hua ZhouDepartment of Neurosurgery, Tianjin Medical University General Hospital, Tianjin 300052, P.R. China.
Shengping YuDepartment of Neurosurgery, Tianjin Medical University General Hospital, Tianjin 300052, P.R. China.
Xuejun YangDepartment of Neurosurgery, Tianjin Medical University General Hospital, Tianjin 300052, P.R. China.
Tianjin Medical University General Hospital · CNAffiliated Hospital of Qingdao University · CNCangzhou Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma multiforme (GBM), WHO grade IV astrocytoma, is the most common primary neoplasm of the central nervous system (CNS) and has the highest malignancy and mortality rates. The invasive nature of GBM complicates surgical resection and restricts chemotherapeutic access, contributing to poor patient prognosis. The migration of tumor cells is closely related to the tumor cell proliferation. The acquisition of migratory capability, in addition to intracellular factors, is proposed to be a crucial mechanism during the progression of invasion. Using qRT-PCR analysis, we determined that the expression of miR-451 in glioma tissue was lower than in control brain tissue, especially in the central portions of the tumor. In glioma cell lines, we found that decreased miR-451 expression suppressed tumor cell proliferation but enhanced migration with a concomitant low level of CAB39/AMPK/mTOR pathway activation and high level of Rac1/cofilin pathway activation, respectively. Notably, the effect of miR-451 on cytological behavior and on the activation of mTOR and Rac1 was limited when AMPKα1 expression was knocked-down with a synthetic shRNA. We suggest that the glioma microenvironment results in heterogeneity of miR-451 expression. Our data indicated that miR-451 relays environmental signals by upregulating the activity of AMPK signaling, thereby modulating the activation of mTOR and Rac1/cofilin which, in turn, play key roles in glioma cell proliferation and migration, respectively. Our results highlight the need to consider opposing roles of a therapeutic target which, while suppressing tumor cell proliferation, could also promote cell infiltration.

Indexed as

AMP-Activated Protein KinasesCalcium-Binding ProteinsCell Line, TumorCell MovementCell ProliferationCofilin 1Gene Expression Regulation, NeoplasticGliomaHumansMicroRNAsNeoplasm Invasivenessrac1 GTP-Binding ProteinSignal TransductionTOR Serine-Threonine KinasesTumor MicroenvironmentAMP-Activated Protein KinasesCAB39 protein, humanCalcium-Binding ProteinsCofilin 1MicroRNAsMIRN451 microRNA, humanMTOR protein, humanPRKAA1 protein, humanrac1 GTP-Binding ProteinRAC1 protein, humanTOR Serine-Threonine Kinases

Identifiers

PMID28440461
PMCPMC5435333
OpenAlexW2607108152

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.