Evidence map›Paper›PMID 30283018›Full record

ArticleScientific reports2018

Glycerophosphatidylcholine PC(36:1) absence and 3'-phosphoadenylate (pAp) accumulation are hallmarks of the human glioma metabolome.

Wenchen Li, Hongmei Jia, Qi Li, Jiayue Cui, Ri Li, Zhongmei Zou, Xinyu Hong

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.6field-weighted citation impact, top 34% 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

11 citing papers in PubMed, 15 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 4 institutions in 1 country.

Wenchen LiDepartment of Neurosurgical Oncology, The First Hospital of Jilin University, Changchun, PC:130021, China.
Hongmei JiaInstitute of Medicinal Plant Development, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, PC:100191, China.
Qi LiCore Laboratory for Clinical Medical Research, Beijing Tian Tan Hospital, Capital Medical University, Beijing, PC:100050, China.
Jiayue CuiDepartment of Histology and Embryology of Basic Medicine College, Jilin University, Changchun, PC:130021, China.
Ri LiDepartment of Neurosurgical Oncology, The First Hospital of Jilin University, Changchun, PC:130021, China.
Zhongmei ZouInstitute of Medicinal Plant Development, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, PC:100191, China. zmzou@implad.ac.cn.
Xinyu HongDepartment of Neurosurgical Oncology, The First Hospital of Jilin University, Changchun, PC:130021, China. hongxy@jlu.edu.cn.
Jilin University · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNCapital Medical University · CNFirst Hospital of Jilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioma is the most prevalent malignant brain tumor. A comprehensive analysis of the glioma metabolome is still lacking. This study aims to explore new special metabolites in glioma tissues. A non-targeted human glioma metabolomics was performed by UPLC-Q-TOF/MS. The gene expressions of 18 enzymes associated with 3'-phosphoadenylate (pAp) metabolism was examined by qRT-PCR. Those enzymes cover the primary metabolic pathway of pAp. We identified 15 new metabolites (13 lipids and 2 nucleotides) that were significantly different between the glioma and control tissues. Glycerophosphatidylcholine [PC(36:1)] content was high and pAp content was significantly low in the control brain (p  < 0.01). In glioma tissues, PC(36:1) was not detected and pAp content was significantly increased. The gene expressions of 3'-nucleotidases (Inositol monophosphatase (IMPAD-1) and 3'(2'),5'-bisphosphate nucleotidase 1(BPNT-1)) were dramatically down-regulated. Meanwhile, the gene expression of 8 sulfotransferases (SULT), 2 phosphoadenosine phosphosulfate synthases (PAPSS-1 and PAPSS-2) and L-aminoadipate-semialdehyde dehydrogenase-phosphopante-theinyl transferase (AASDHPPT) were up-regulated. PC(36:1) absence and pAp accumulation are the most noticeable metabolic aberration in glioma. The dramatic down-regulation of IMPAD-1 and BPNT-1 are the primary cause for pAp dramatic accumulation. Our findings suggest that differential metabolites discovered in glioma could be used as potentially novel therapeutic targets or diagnostic biomarkers and that abnormal metabolism of lipids and nucleotides play roles in the pathogenesis of glioma.

Indexed as

MetabolomicsAdenosine DiphosphateAdultAgedArylsulfotransferaseFemaleGene Expression Regulation, NeoplasticGliomaHumansMaleMetabolomeMiddle AgedMultienzyme ComplexesNucleotidasesPhosphatidylcholinesSulfate AdenylyltransferaseAdenosine DiphosphateArylsulfotransferaseBPNT1 protein, humanMultienzyme ComplexesNucleotidasesPAPS synthetasePhosphatidylcholinesSulfate Adenylyltransferase

Identifiers

PMID30283018
PMCPMC6170378
OpenAlexW2893064205

What OpenQuestion holds

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LicenceCC BY
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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.