Evidence map›Paper›PMID 25760394›Full record

ArticleMolecular medicine reports2015

All-trans retinoic acid impairs the vasculogenic mimicry formation ability of U87 stem-like cells through promoting differentiation.

Geng-Qiang Ling, Yi-Jing Liu, Yi-Quan Ke, Lei Chen, Xiao-Dan Jiang, Chuan-Lu Jiang, Wei Ye

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

13 citing papers in PubMed, 28 citations in OpenAlex.

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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

7 authors at 3 institutions in 1 country.

Geng-Qiang LingDepartment of Neurosurgery, Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150086, P.R. China.
Yi-Jing LiuDepartment of Neurosurgery, Zhujiang Hospital, National Key Clinic Department, Neurosurgery Institute, Key Laboratory on Brain Function Repair and Regeneration of Guangdong, Southern Medical University, Guangzhou, Guangdong 510282, P.R. China.
Yi-Quan KeDepartment of Neurosurgery, Zhujiang Hospital, National Key Clinic Department, Neurosurgery Institute, Key Laboratory on Brain Function Repair and Regeneration of Guangdong, Southern Medical University, Guangzhou, Guangdong 510282, P.R. China.
Lei ChenDepartment of Neurosurgery, Zhujiang Hospital, National Key Clinic Department, Neurosurgery Institute, Key Laboratory on Brain Function Repair and Regeneration of Guangdong, Southern Medical University, Guangzhou, Guangdong 510282, P.R. China.
Xiao-Dan JiangDepartment of Neurosurgery, Zhujiang Hospital, National Key Clinic Department, Neurosurgery Institute, Key Laboratory on Brain Function Repair and Regeneration of Guangdong, Southern Medical University, Guangzhou, Guangdong 510282, P.R. China.
Chuan-Lu JiangDepartment of Neurosurgery, Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150086, P.R. China.
Wei YeDepartment of Neurosurgery, Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150086, P.R. China.
Second Affiliated Hospital of Harbin Medical University · CNSouthern Medical University · CNZhujiang Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The poor therapeutic effect of traditional antiangiogenic therapy on glioblastoma multiforme (GBM) may be attributed to vasculogenic mimicry (VM), which was previously reported to be promoted by cancer stem-like cells (SLCs). All-trans retinoic acid (ATRA), a potent reagent which drives differentiation, was reported to be able to eradicate cancer SLCs in certain malignancies. The aim of the present study was to investigate the effects of ATRA on the VM formation ability of U87 glioblastoma SLCs. The expression of cancer SLC markers CD133 and nestin was detected using immunocytochemistry in order to identify U87 SLCs. In addition, the differentiation of these SLCs was observed through detecting the expression of glial fibrillary acidic protein (GFAP), β-tubulin III and galactosylceramidase (Galc) using immunofluorescent staining. The results showed that the expression levels of GFAP, β-tubulin III and Galc were upregulated following treatment with ATRA in a dose-dependent manner. Furthermore, ATRA significantly reduced the proliferation, invasiveness, tube formation and vascular endothelial growth factor (VEGF) secretion of U87 SLCs. In conclusion, the VM formation ability of SLCs was found to be negatively correlated with differentiation. These results therefore suggested that ATRA may serve as a promising novel agent for the treatment of GBM due to its role in reducing VM formation.

Indexed as

AC133 AntigenAngiogenesis InhibitorsAntigens, CDBiomarkers, TumorCell DifferentiationCell Line, TumorCell MovementCell ProliferationDose-Response Relationship, DrugGalactosylceramidaseGene ExpressionGlial Fibrillary Acidic ProteinGlycoproteinsHumansNeoplastic Stem CellsNeovascularization, PathologicAC133 AntigenAngiogenesis InhibitorsAntigens, CDBiomarkers, TumorGalactosylceramidaseGlial Fibrillary Acidic ProteinGlycoproteinsNES protein, humanNestinPeptidesPROM1 protein, humanTretinoinTUBB3 protein, humanTubulinVascular Endothelial Growth Factor AVEGFA protein, human

Identifiers

PMID25760394
PMCPMC4438921
OpenAlexW2098104354

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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.