Evidence map›Paper›PMID 25015090›Full record

ArticleNeuro-oncology2014

Functional analysis of a novel glioma antigen, EFTUD1.

Katsuya Saito, Yukihiko Iizuka, Shigeki Ohta, Satoshi Takahashi, Kenta Nakamura, Hideyuki Saya, Kazunari Yoshida, Yutaka Kawakami, Masahiro Toda

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

Article in Neuro-oncology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
0.9field-weighted citation impact, top 26% 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

6 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
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 1 institution in 1 country.

Katsuya SaitoDepartment of Neurosurgery, Keio University School of Medicine, Tokyo, Japan (K.S., S.T., K.Y., M.T.); Neuro-immunology Research Group, Keio University School of Medicine, Tokyo, Japan (Y.I., S.O., M.T.); Department of Physiology, Keio University School of Medicine, Tokyo, Japan (S.O.); Division of Cellular Signaling, Institute for Advanced Medical Research, Keio University School of Medicine, Tokyo, Japan (K.N., Y.K.); Division of Gene Regulation, Institute for Advanced Medical Research, Keio University School of Medicine, Tokyo, Japan (H.S.).
Yukihiko IizukaDepartment of Neurosurgery, Keio University School of Medicine, Tokyo, Japan (K.S., S.T., K.Y., M.T.); Neuro-immunology Research Group, Keio University School of Medicine, Tokyo, Japan (Y.I., S.O., M.T.); Department of Physiology, Keio University School of Medicine, Tokyo, Japan (S.O.); Division of Cellular Signaling, Institute for Advanced Medical Research, Keio University School of Medicine, Tokyo, Japan (K.N., Y.K.); Division of Gene Regulation, Institute for Advanced Medical Research, Keio University School of Medicine, Tokyo, Japan (H.S.).
Shigeki OhtaDepartment of Neurosurgery, Keio University School of Medicine, Tokyo, Japan (K.S., S.T., K.Y., M.T.); Neuro-immunology Research Group, Keio University School of Medicine, Tokyo, Japan (Y.I., S.O., M.T.); Department of Physiology, Keio University School of Medicine, Tokyo, Japan (S.O.); Division of Cellular Signaling, Institute for Advanced Medical Research, Keio University School of Medicine, Tokyo, Japan (K.N., Y.K.); Division of Gene Regulation, Institute for Advanced Medical Research, Keio University School of Medicine, Tokyo, Japan (H.S.).
Satoshi TakahashiDepartment of Neurosurgery, Keio University School of Medicine, Tokyo, Japan (K.S., S.T., K.Y., M.T.); Neuro-immunology Research Group, Keio University School of Medicine, Tokyo, Japan (Y.I., S.O., M.T.); Department of Physiology, Keio University School of Medicine, Tokyo, Japan (S.O.); Division of Cellular Signaling, Institute for Advanced Medical Research, Keio University School of Medicine, Tokyo, Japan (K.N., Y.K.); Division of Gene Regulation, Institute for Advanced Medical Research, Keio University School of Medicine, Tokyo, Japan (H.S.).
Kenta NakamuraDepartment of Neurosurgery, Keio University School of Medicine, Tokyo, Japan (K.S., S.T., K.Y., M.T.); Neuro-immunology Research Group, Keio University School of Medicine, Tokyo, Japan (Y.I., S.O., M.T.); Department of Physiology, Keio University School of Medicine, Tokyo, Japan (S.O.); Division of Cellular Signaling, Institute for Advanced Medical Research, Keio University School of Medicine, Tokyo, Japan (K.N., Y.K.); Division of Gene Regulation, Institute for Advanced Medical Research, Keio University School of Medicine, Tokyo, Japan (H.S.).
Hideyuki SayaDepartment of Neurosurgery, Keio University School of Medicine, Tokyo, Japan (K.S., S.T., K.Y., M.T.); Neuro-immunology Research Group, Keio University School of Medicine, Tokyo, Japan (Y.I., S.O., M.T.); Department of Physiology, Keio University School of Medicine, Tokyo, Japan (S.O.); Division of Cellular Signaling, Institute for Advanced Medical Research, Keio University School of Medicine, Tokyo, Japan (K.N., Y.K.); Division of Gene Regulation, Institute for Advanced Medical Research, Keio University School of Medicine, Tokyo, Japan (H.S.).
Kazunari YoshidaDepartment of Neurosurgery, Keio University School of Medicine, Tokyo, Japan (K.S., S.T., K.Y., M.T.); Neuro-immunology Research Group, Keio University School of Medicine, Tokyo, Japan (Y.I., S.O., M.T.); Department of Physiology, Keio University School of Medicine, Tokyo, Japan (S.O.); Division of Cellular Signaling, Institute for Advanced Medical Research, Keio University School of Medicine, Tokyo, Japan (K.N., Y.K.); Division of Gene Regulation, Institute for Advanced Medical Research, Keio University School of Medicine, Tokyo, Japan (H.S.).
Yutaka KawakamiDepartment of Neurosurgery, Keio University School of Medicine, Tokyo, Japan (K.S., S.T., K.Y., M.T.); Neuro-immunology Research Group, Keio University School of Medicine, Tokyo, Japan (Y.I., S.O., M.T.); Department of Physiology, Keio University School of Medicine, Tokyo, Japan (S.O.); Division of Cellular Signaling, Institute for Advanced Medical Research, Keio University School of Medicine, Tokyo, Japan (K.N., Y.K.); Division of Gene Regulation, Institute for Advanced Medical Research, Keio University School of Medicine, Tokyo, Japan (H.S.).
Masahiro TodaDepartment of Neurosurgery, Keio University School of Medicine, Tokyo, Japan (K.S., S.T., K.Y., M.T.); Neuro-immunology Research Group, Keio University School of Medicine, Tokyo, Japan (Y.I., S.O., M.T.); Department of Physiology, Keio University School of Medicine, Tokyo, Japan (S.O.); Division of Cellular Signaling, Institute for Advanced Medical Research, Keio University School of Medicine, Tokyo, Japan (K.N., Y.K.); Division of Gene Regulation, Institute for Advanced Medical Research, Keio University School of Medicine, Tokyo, Japan (H.S.).
Keio University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundA cDNA library made from 2 glioma cell lines, U87MG and T98G, was screened by serological identification of antigens by recombinant cDNA expression (SEREX) using serum from a glioblastoma patient. Elongation factor Tu GTP binding domain containing protein 1 (EFTUD1), which is required for ribosome biogenesis, was identified. A cancer microarray database showed overexpression of EFTUD1 in gliomas, suggesting that EFTUD1 is a candidate molecular target for gliomas.

methodsEFTUD1 expression in glioma cell lines and glioma tissue was assessed by Western blot, quantitative PCR, and immunohistochemistry. The effect on ribosome biogenesis, cell growth, cell cycle, and induction of apoptosis and autophagy in glioma cells during the downregulation of EFTUD1 was investigated. To reveal the role of autophagy, the autophagy-blocker, chloroquine (CQ), was used in glioma cells downregulating EFTUD1. The effect of combining CQ with EFTUD1 inhibition in glioma cells was analyzed.

resultsEFTUD1 expression in glioma cell lines and tissue was higher than in normal brain tissue. Downregulating EFTUD1 induced G1 cell-cycle arrest and apoptosis, leading to reduced glioma cell proliferation. The mechanism underlying this antitumor effect was impaired ribosome biogenesis via EFTUD1 inhibition. Additionally, protective autophagy was induced by glioma cells as an adaptive response to EFTUD1 inhibition. The antitumor effect induced by the combined treatment was significantly higher than that of either EFTUD1 inhibition or CQ alone.

conclusionThese results suggest that EFTUD1 represents a novel therapeutic target and that the combination of EFTUD1 inhibition with autophagy blockade may be effective in the treatment of gliomas.

Indexed as

Antigens, NeoplasmApoptosisAutophagyBrain NeoplasmsCell CycleCell Line, TumorDown-RegulationEukaryotic Initiation FactorsGene LibraryGliomaHumansPeptide Elongation FactorsRibonucleoprotein, U5 Small NuclearRibosomesAntigens, NeoplasmEFL1 protein, humanEIF6 protein, humanEukaryotic Initiation FactorsPeptide Elongation FactorsRibonucleoprotein, U5 Small NuclearautophagyEFTUD1gliomaribosome biogenesisSEREX

Identifiers

PMID25015090
PMCPMC4232085
OpenAlexW2027398659

What OpenQuestion holds

Textmetadata
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.