Evidence map›Paper›PMID 26259235›Full record

ArticleOncotarget2015

PERK/CHOP contributes to the CGK733-induced vesicular calcium sequestration which is accompanied by non-apoptotic cell death.

Yufeng Wang, Yasuhiro Kuramitsu, Byron Baron, Takao Kitagawa, Junko Akada, Kazuhiro Tokuda, Dan Cui, Kazuyuki Nakamura

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. 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
0.8field-weighted citation impact, top 31% 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, 19 citations in OpenAlex.

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  10. TNFα induces CaJournal of experimental & clinical cancer research : CR · 2018
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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

8 authors at 2 institutions in 1 country.

Yufeng WangDepartment of Biochemistry and Functional Proteomics, Yamguchi University Graduate School of Medicine, Ube, Japan.
Yasuhiro KuramitsuDepartment of Biochemistry and Functional Proteomics, Yamguchi University Graduate School of Medicine, Ube, Japan.
Byron BaronDepartment of Biochemistry and Functional Proteomics, Yamguchi University Graduate School of Medicine, Ube, Japan.
Takao KitagawaDepartment of Biochemistry and Functional Proteomics, Yamguchi University Graduate School of Medicine, Ube, Japan.
Junko AkadaDepartment of Biochemistry and Functional Proteomics, Yamguchi University Graduate School of Medicine, Ube, Japan.
Kazuhiro TokudaDepartment of Biochemistry and Functional Proteomics, Yamguchi University Graduate School of Medicine, Ube, Japan.
Dan CuiDepartment of Pathology, Yamguchi University Graduate School of Medicine, Ube, Japan.
Kazuyuki NakamuraDepartment of Biochemistry and Functional Proteomics, Yamguchi University Graduate School of Medicine, Ube, Japan.
Yamaguchi University · JPTokuyama (Japan) · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Calcium ions (Ca(2+)) are indispensable for the physiology of organisms and the molecular regulation of cells. We observed that CGK733, a synthetic chemical substance, induced non-apoptotic cell death and stimulated reversible calcium sequestration by vesicles in pancreatic cancer cells. The endoplasmic reticulum (ER) stress eukaryotic translation initiation factor 2-alpha kinase 3/C/EBP homologous protein (PERK/CHOP) signaling pathway was shown to be activated by treatment with CGK733. Ionomycin, an ER stress drug and calcium ionophore, can activate PERK/CHOP signaling and accelerate CGK733-induced calcium sequestration. Knockdown of CHOP diminished CGK733-induced vesicular calcium sequestration, but had no effects on the cell death. Proteomic analysis demonstrated that the ER-located calcium-binding proteins, calumenin and protein S100-A11, were altered in CGK733-treated cells compared to non-treated controls. Our study reveals that CGK733-induced intracellular calcium sequestration is correlated with the PERK/CHOP signaling pathway and may also be involved in the dysregulations of calcium-binding proteins.

Indexed as

Antineoplastic AgentsBenzeneacetamidesCalciumCalcium-Binding ProteinsCalcium IonophoresCell DeathCell Line, TumorDose-Response Relationship, DrugeIF-2 KinaseEndoplasmic ReticulumHumansPancreatic NeoplasmsProteomicsRNA InterferenceS100 ProteinsSignal TransductionAntineoplastic AgentsBenzeneacetamidesCalciumCalcium-Binding ProteinsCalcium IonophoresCALU protein, humanCGK 733DDIT3 protein, humanEIF2AK3 protein, humaneIF-2 KinaseS100A11 protein, humanS100 ProteinsThioureaTranscription Factor CHOPcalcium sequestrationCGK733ER stressnon-apoptotic deathPERK/CHOP

Identifiers

PMID26259235
PMCPMC4694829
OpenAlexW1579972932

What OpenQuestion holds

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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.