Evidence map›Paper›PMID 24057885›Full record

ArticleNeuro-oncology2013

Mitochondrial protein ATPase family, AAA domain containing 3A correlates with radioresistance in glioblastoma.

Weir-Chiang You, Shiow-Her Chiou, Chih-Yang Huang, Shu-Fen Chiang, Cheng-Lin Yang, Janaki N Sudhakar, Tze-Yi Lin, I-Ping Chiang, Chiung-Chyi Shen, Wen-Yu Cheng and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Neuro-oncology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
0.7field-weighted citation impact, top 27% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. ATAD3A: A Key Regulator of Mitochondria-Associated Diseases.International journal of molecular sciences · 2023
    Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Emerging Links between Control of Mitochondrial Protein ATAD3A and Cancer.International journal of molecular sciences · 2020
    Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Role of metabolism in cancer cell radioresistance and radiosensitization methods.Journal of experimental & clinical cancer research : CR · 2018
    Review
  18. Article
  19. Article
  20. Review
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

13 authors at 7 institutions in 1 country.

Weir-Chiang YouCorresponding Author: Kuan-Chih Chow, PhD, Graduate Institute of Biomedical Sciences, National Chung Hsing University, 250 Kuo-Kuang Road, Taichung 40227, Taiwan. kcchow@dragon.nchu.edu.tw.
Shiow-Her Chiou
Chih-Yang Huang
Shu-Fen Chiang
Cheng-Lin Yang
Janaki N Sudhakar
Tze-Yi Lin
I-Ping Chiang
Chiung-Chyi Shen
Wen-Yu Cheng
Jin-Chin Lin
Shwn-Huey Shieh
Kuan-Chih Chow
China Medical University · TWHungkuang University · TWMinistry of Health and Welfare · TWNational Chung Hsing University · TWNational Yang Ming Chiao Tung University · TWChina Medical University Hospital · TWTaichung Veterans General Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundATPase-family, AAA domain containing 3A (ATAD3A) is located on human chromosome 1p36.33, and high endogenous expression may associate with radio- and chemosensitivity. This study was conducted to investigate the significance of ATAD3A in glioblastoma multiforme (GBM).

methodsClinical significance of ATAD3A expression was assessed by immunohistochemistry in 67 GBM specimens, and prognostic value was assessed in 32 GBM patients statistically. To investigate in vitro phenotypic effects of ATAD3A, cell viability was measured using a clonogenic survival assay under either knockdown or ectopic expression of ATAD3A in GBM cell lines. The effects of ATAD3A knockdown on targeted DNA repair-associated proteins in T98G cells were evaluated using immunofluorescence and Western blotting.

resultsClinically, high expression of ATAD3A was independent of O(6)-DNA methylguanine-methyltransferase methylation status and correlated with worse prognosis. In vitro, high ATAD3A-expressing T98G cells were more resistant to radiation-induced cell death compared with control and low endogenous ATAD3A U87MG cells. After silencing ATAD3A, T98G cells became more sensitive to radiation. On the other hand, enforced ATAD3A expression in U87MG cells exhibited increased radioresistance. ATAD3A may coordinate with aldo-keto reductase genes and participate in bioactivation or detoxication of temozolomide. Surprisingly, deficient DNA repair after irradiation was observed in T98G/ATAD3A knockdown as a result of decreased nuclear ataxia telangiectasia mutated kinase and histones H2AX and H3, which was also evidenced by the sustained elevation of poly (ADP-ribose) polymerase prior to and after radiation treatment.

conclusionOur data suggest that high expression of ATAD3A is an independent biomarker for radioresistance in GBM. ATAD3A could be a potential target for therapy.

Indexed as

Radiation ToleranceAdenosine TriphosphatasesAntineoplastic Agents, AlkylatingATPases Associated with Diverse Cellular ActivitiesBlotting, WesternBrain NeoplasmsCell DifferentiationCell ProliferationChemoradiotherapyDacarbazineDNA MethylationFemaleGene Expression Regulation, NeoplasticGlioblastomaHumansImmunoenzyme TechniquesAdenosine TriphosphatasesAntineoplastic Agents, AlkylatingATAD3A protein, humanATPases Associated with Diverse Cellular ActivitiesDacarbazineMembrane ProteinsMitochondrial ProteinsO(6)-Methylguanine-DNA MethyltransferaseRNA, MessengerRNA, Small InterferingTemozolomideATAD3AautophagyDNA repairglioblastoma multiformeradiation

Identifiers

PMID24057885
PMCPMC3779036
OpenAlexW2163665758

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.