Evidence map›Paper›PMID 29867331›Full record

ArticleFrontiers in neuroscience2018

Activity of Metabotropic Glutamate Receptor 4 Suppresses Proliferation and Promotes Apoptosis With Inhibition of Gli-1 in Human Glioblastoma Cells.

Zhichao Zhang, Xiaoyan Zheng, Yan Luan, Yingfei Liu, Xingxing Li, Chongxiao Liu, Haixia Lu, Xinlin Chen, Yong Liu

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 14% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.

  1. Pooled it
  2. Inhibitory glutamatergic feedback for brain tumor therapy.Medical oncology (Northwood, London, England) · 2026
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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

9 authors at 2 institutions in 1 country.

Zhichao ZhangInstitute of Neurobiology, Xi'an Jiaotong University Health Science Center, Xi'an, China.
Xiaoyan ZhengInstitute of Neurobiology, Xi'an Jiaotong University Health Science Center, Xi'an, China.
Yan LuanInstitute of Neurobiology, Xi'an Jiaotong University Health Science Center, Xi'an, China.
Yingfei LiuInstitute of Neurobiology, Xi'an Jiaotong University Health Science Center, Xi'an, China.
Xingxing LiInstitute of Neurobiology, Xi'an Jiaotong University Health Science Center, Xi'an, China.
Chongxiao LiuInstitute of Neurobiology, Xi'an Jiaotong University Health Science Center, Xi'an, China.
Haixia LuInstitute of Neurobiology, Xi'an Jiaotong University Health Science Center, Xi'an, China.
Xinlin ChenInstitute of Neurobiology, Xi'an Jiaotong University Health Science Center, Xi'an, China.
Yong LiuInstitute of Neurobiology, Xi'an Jiaotong University Health Science Center, Xi'an, China.
Xi'an Jiaotong University · CNSecond Affiliated Hospital of Xi'an Jiaotong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma multiforme (GBM) is the most lethal glioma variant in the adult brain and among the deadliest of human cancers. Increasing evidence has shown that metabotropic glutamate receptor subtype 4 (mGluR4) expression may play roles in regulating the growth of neural stem cells as well as several cancer cell lines. Here, we investigated the effects of mGluR4 on the growth and apoptosis of the LN229 GBM cell line. Involvement of Gli-1, one of the key transcription factors in the sonic Hedgehog (SHH) signaling pathway, was further explored. In this study, mGluR4 was activated using selective agonist VU0155041; and gene-targeted siRNAs were used to generate loss of function of mGluR4 and Gli-1 in LN229 cells. The results demonstrated that LN229 cells expressed mGluR4 and the agonist VU0155041 decreased cell viability in a dose- and time-dependent manner. Activation of mGluR4 inhibited cyclin D1 expression, activated pro-caspase-8/9/3, and disrupted the balance of Bcl-2/Bax expression, which indicated cell cycle arrest and apoptosis of LN229 cells, respectively. Furthermore, Gli-1 expression was reduced by mGluR4 activation in LN229 cells, and downregulation of Gli-1 expression by gene-targeted siRNA resulted in both inhibition of cell proliferation and promotion of apoptosis. Moreover, VU0155041 treatment substantially blocked SHH-induced cyclin D1 expression and cell proliferation, while increasing TUNEL-positive cells and the activation of apoptosis-related proteins. We concluded that activation of mGluR4 expressed in LN229 cells could inhibit GBM cell growth by decreasing cell proliferation and promoting apoptosis. Further suppression of intracellular Gli-1 expression might be involved in the action of mGluR4 on cancer cells. Our study suggested a novel role of mGluR4, which might serve as a potential drug target for control of GBM cell growth.

Indexed as

apoptosisGli-1glioblastoma multiformeLN229 cellsmetabotropic glutamate receptor 4proliferation

Identifiers

PMID29867331
PMCPMC5962807
OpenAlexW2800051819

What OpenQuestion holds

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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.