Evidence map›Paper›PMID 27166188›Full record

ArticleOncotarget2016

The mechanisms of malic enzyme 2 in the tumorigenesis of human gliomas.

Chiao-Pei Cheng, Li-Chun Huang, Yung-Lung Chang, Ching-Hsuan Hsieh, Shih-Ming Huang, Dueng-Yuan Hueng

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

17 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Review
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  4. Targeting human mitochondrial NAD(P)Cellular oncology (Dordrecht, Netherlands) · 2023
    Article
  5. Article
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  11. Mitochondrial malic enzyme 2 promotes breast cancer metastasis via stabilizing HIF-1α under hypoxia.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2021
    Article
  12. Review
  13. 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

6 authors at 2 institutions in 1 country.

Chiao-Pei ChengGraduate Institute of Medical Sciences, National Defense Medical Center, Taipei, Taiwan, ROC.
Li-Chun HuangDepartment of Biochemistry, National Defense Medical Center, Taipei, Taiwan, ROC.
Yung-Lung ChangDepartment of Biochemistry, National Defense Medical Center, Taipei, Taiwan, ROC.
Ching-Hsuan HsiehDepartment of Neurological Surgery, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan, ROC.
Shih-Ming HuangGraduate Institute of Medical Sciences, National Defense Medical Center, Taipei, Taiwan, ROC.
Dueng-Yuan HuengGraduate Institute of Medical Sciences, National Defense Medical Center, Taipei, Taiwan, ROC.
National Defense Medical Center · TWTri-Service General Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The high level of resistance of glioblastoma multiforme (GBM) to currently used chemotherapies and other conventional therapies, its invasive characteristics and the presence of stem-like cells are the major factors that make the treatment of GBM difficult. Recent studies have demonstrated that the homeostasis of energy metabolism, glycolysis and mitochondrial oxidation of glucose are important for GBM cell growth and chemo-resistance. However, it is not clear which specific gene(s) are involved in the homeostasis of energy metabolism and invasiveness of GBM cells. We performed a preliminary analysis of data obtained from Gene Expression Omnibus profiles and determined that malic enzyme 2 (ME2) expression was positively associated with WHO grade in human primary gliomas. Hence, we evaluated the detailed working mechanisms of ME2 in human GBM cell processes, including proliferation, cell cycle, invasion, migration, ROS, and ATP production. Our data demonstrated that ME2 was involved in GBM growth, invasion and migration. ME2 has two cofactors, NAD+ or NADP+, which are used to produce NADH and NADPH for ATP production and ROS clearance, respectively. If the catalytic activity of ME2 is determined to be critical for its roles in GBM growth, invasion and migration, small molecule inhibitors of ME2 may be valuable drugs for GBM therapy. We hope that our current data provides a candidate treatment strategy for GBM.

Indexed as

Adenosine TriphosphateBrain NeoplasmsCarcinogenesisCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, EnzymologicGene Expression Regulation, NeoplasticGlioblastomaGliomaHumansMalate DehydrogenaseReactive Oxygen SpeciesRNA, Small InterferingAdenosine TriphosphateMalate Dehydrogenasemalic enzyme 2; humanReactive Oxygen SpeciesRNA, Small Interferingglioblastoma multiformemalic enzyme 2p53reactive oxygen speciestumorigenesis

Identifiers

PMID27166188
PMCPMC5173072
OpenAlexW2347057298

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.