Evidence map›Paper›PMID 24626062›Full record

ArticleCancer gene therapy2014

14-3-3 eta depletion sensitizes glioblastoma cells to irradiation due to enhanced mitotic cell death.

G-Y Park, J Y Han, Y K Han, S D Kim, J S Kim, W S Jo, S H Chun, D H Jeong, C-W Lee, K Yang and 1 more

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Cancer gene therapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
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  4. Metabolomics and Proteomics Reveal the Variation of Substances in Apheresis Platelets during Storage and Their Effects on Cancer Cell Proliferation.Transfusion medicine and hemotherapy : offizielles Organ der Deutschen Gesellschaft fur Transfusionsmedizin und Immunhamatologie · 2021
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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

11 authors at 2 institutions in 1 country.

G-Y Park1] Research Center, Dongnam Institute of Radiological & Medical Sciences, Busan, ROK [2] Department of Biological Sciences, Pusan National University, Busan, ROK.
J Y HanResearch Center, Dongnam Institute of Radiological & Medical Sciences, Busan, ROK.
Y K HanResearch Center, Dongnam Institute of Radiological & Medical Sciences, Busan, ROK.
S D KimResearch Center, Dongnam Institute of Radiological & Medical Sciences, Busan, ROK.
J S KimResearch Center, Dongnam Institute of Radiological & Medical Sciences, Busan, ROK.
W S JoResearch Center, Dongnam Institute of Radiological & Medical Sciences, Busan, ROK.
S H ChunResearch Center, Dongnam Institute of Radiological & Medical Sciences, Busan, ROK.
D H JeongResearch Center, Dongnam Institute of Radiological & Medical Sciences, Busan, ROK.
C-W Lee1] Department of Molecular Cell Biology, Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Suwon, ROK [2] Center for Molecular Medicine, Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Suwon, ROK [3] Samsung Advanced Institute for Health Sciences and Technology, Sungkyunkwan University, Suwon, ROK.
K Yang1] Research Center, Dongnam Institute of Radiological & Medical Sciences, Busan, ROK [2] Department of Radiation Oncology, Dongnam Institute of Radiological & Medical Sciences, Busan, ROK [3] Department of Radiation Oncology, Korea Institute of Radiological & Medical Sciences, Seoul, ROK.
C G LeeResearch Center, Dongnam Institute of Radiological & Medical Sciences, Busan, ROK.
Dongnam Institute of Radiological & Medical Sciences · KRSamsung (South Korea) · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

14-3-3 proteins have important roles in several cellular processes such as cell cycle progression, the DNA-damage checkpoint and apoptosis. We have shown previously that depleting 14-3-3η, a 14-3-3 isoform, enhances mitotic cell death, and that combining it with microtubule agents is more effective for anticancer therapeutics. In this study, we investigated whether depleting 14-3-3η can be combined with radiotherapy to enhance its therapeutic efficacy. We found that depleting 14-3-3η resulted in a synergistic radiosensitizing effect when combined with radiotherapy in several glioblastoma cell lines, where its specific expression and correlation of its expression level with malignancy have been reported. The radiosensitizing effect was associated with enhanced mitotic cell death by 14-3-3η depletion but not with mitotic catastrophe, which is one of the major cell death mechanisms observed in response to irradiation of most solid tumors. These results suggest that 14-3-3η may be a therapeutic target to overcome radioresistance in glioblastoma.

Indexed as

14-3-3 ProteinsApoptosisBrain NeoplasmsCell CycleCell DeathCell Growth ProcessesCell Line, TumorCell SurvivalGlioblastomaHeLa CellsHumansMitosisRadiation ToleranceRNA, Small InterferingTransfection14-3-3 ProteinsRNA, Small InterferingYWHAH protein, human

Identifiers

PMID24626062
OpenAlexW1988910291

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.