Evidence map›Paper›PMID 29843637›Full record

ArticleBMC cancer2018

ARL2 overexpression inhibits glioma proliferation and tumorigenicity via down-regulating AXL.

Yulin Wang, Gefei Guan, Wen Cheng, Yang Jiang, Fengping Shan, Anhua Wu, Peng Cheng, Zongze Guo

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 16% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.

  1. Pooled it
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  5. CircLRFN5 inhibits the progression of glioblastoma via PRRX2/GCH1 mediated ferroptosis.Journal of experimental & clinical cancer research : CR · 2022
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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

8 authors at 2 institutions in 1 country.

Yulin WangDepartment of Neurosurgery, The First Hospital of China Medical University, 155 Nanjingbei Street, Heping, Shenyang, Liaoning, 110001, People's Republic of China.
Gefei GuanDepartment of Neurosurgery, The First Hospital of China Medical University, 155 Nanjingbei Street, Heping, Shenyang, Liaoning, 110001, People's Republic of China.
Wen ChengDepartment of Neurosurgery, The First Hospital of China Medical University, 155 Nanjingbei Street, Heping, Shenyang, Liaoning, 110001, People's Republic of China.
Yang JiangDepartment of Neurosurgery, The First Hospital of China Medical University, 155 Nanjingbei Street, Heping, Shenyang, Liaoning, 110001, People's Republic of China.
Fengping ShanDepartment of Immunology, School of Basic Medical Science, China Medical University, Shenyang, 110122, Liaoning, China.
Anhua WuDepartment of Neurosurgery, The First Hospital of China Medical University, 155 Nanjingbei Street, Heping, Shenyang, Liaoning, 110001, People's Republic of China.
Peng ChengDepartment of Neurosurgery, The First Hospital of China Medical University, 155 Nanjingbei Street, Heping, Shenyang, Liaoning, 110001, People's Republic of China. chengpengcmu@sina.com.ORCID http://orcid.org/0000-0003-0626-7040
Zongze GuoDepartment of Neurosurgery, The First Hospital of China Medical University, 155 Nanjingbei Street, Heping, Shenyang, Liaoning, 110001, People's Republic of China. cmuguozongze@163.com.
First Hospital of China Medical University · CNChina Medical University · CN

Funding

Liaoning Science and Technology Plan Projects 2012225014Liaoning Science and Technology Plan Projects 2012225070Natural Science Foundation of China 30901781
6 · The paper itself

Abstract

backgroundGlioma is the most common primary brain tumor in adults with a poor prognosis. As a member of ARF subfamily GTPase, ARL2 plays a key role in regulating the dynamics of microtubules and mitochondrial functions. Recently, ARL2 has been identified as a prognostic and therapeutic target in a variety range of malignant tumors. However, the biological functional role of ARL2 in glioma still remains unknown. The aim of this study was to explore the expression and functional role of ARL2 in glioma.

methodsIn this study, we investigated the expression of ARL2 in glioma samples by using RT-PCR, immunohistochemistry and western blot. The correlation between ARL2 expression and the outcomes of glioma patients was evaluated with survival data from TCGA, CGGA and Rembrandt dataset. Lentiviral technique was used for ARL2 overexpression in U87 and U251 cells. CCK8 assay, colony formation assay, wound healing test, transwell invasion assay and in vivo subcutaneous xenograft model were performed to investigated the biological functions of ARL2.

resultsARL2 expression was down-regulated in glioma, and was inversely associated with poor prognosis in glioma patients. Furthermore, exogenous ARL2 overexpression attenuated the growth and colony-formation abilities of glioma cells, as well as their migration and invasive capabilities. Moreover, elevated expression of ARL2 inhibited in vivo tumorigenicity of glioma cells. Mechanistically, ARL2 regulated AXL expression, which was known as an important functional regulator of proliferation and tumorigenicity in glioma cells.

conclusionOur study suggests that ARL2 inhibits the proliferation, migration and tumorigenicity of glioma cells by regulating the expression of AXL and may conduct as a new prognostic and therapeutic target for glioma.

Indexed as

AnimalsAxl Receptor Tyrosine KinaseBrainBrain NeoplasmsCell Line, TumorCell MovementCell ProliferationDatasets as TopicDown-RegulationFemaleGliomaGTP-Binding ProteinsHumansMaleMice, Inbred BALB CMice, NudeARL2 protein, humanAxl Receptor Tyrosine KinaseGTP-Binding ProteinsProto-Oncogene ProteinsReceptor Protein-Tyrosine KinasesARL2AXLBrain cancerGliomaTumorgenecity

Identifiers

PMID29843637
PMCPMC5975491
OpenAlexW2807184338

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.