Evidence map›Paper›PMID 24971999›Full record

ArticlePloS one2014

Gefitinib and luteolin cause growth arrest of human prostate cancer PC-3 cells via inhibition of cyclin G-associated kinase and induction of miR-630.

Minami A Sakurai, Yuki Ozaki, Daisuke Okuzaki, Yoko Naito, Towa Sasakura, Ayumi Okamoto, Hiroe Tabara, Takao Inoue, Man Hagiyama, Akihiko Ito and 2 more

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

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
4.6field-weighted citation impact, top 4% 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

40 citing papers in PubMed, 94 citations in OpenAlex.

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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

12 authors at 2 institutions in 1 country.

Minami A SakuraiDepartment of Molecular Genetics, Osaka University, Suita City, Osaka, Japan.
Yuki OzakiDepartment of Molecular Genetics, Osaka University, Suita City, Osaka, Japan.
Daisuke OkuzakiDepartment of Molecular Genetics, Osaka University, Suita City, Osaka, Japan; DNA-chip Development Center for Infectious Diseases, Research Institute for Microbial Diseases, Osaka University, Suita City, Osaka, Japan.
Yoko NaitoDepartment of Molecular Genetics, Osaka University, Suita City, Osaka, Japan.
Towa SasakuraDepartment of Molecular Genetics, Osaka University, Suita City, Osaka, Japan.
Ayumi OkamotoDepartment of Molecular Genetics, Osaka University, Suita City, Osaka, Japan.
Hiroe TabaraDepartment of Molecular Genetics, Osaka University, Suita City, Osaka, Japan.
Takao InoueDepartment of Pathology, Faculty of Medicine, Kinki University, Osaka-Sayama, Osaka, Japan.
Man HagiyamaDepartment of Pathology, Faculty of Medicine, Kinki University, Osaka-Sayama, Osaka, Japan.
Akihiko ItoDepartment of Pathology, Faculty of Medicine, Kinki University, Osaka-Sayama, Osaka, Japan.
Norikazu YabutaDepartment of Molecular Genetics, Osaka University, Suita City, Osaka, Japan.
Hiroshi NojimaDepartment of Molecular Genetics, Osaka University, Suita City, Osaka, Japan; DNA-chip Development Center for Infectious Diseases, Research Institute for Microbial Diseases, Osaka University, Suita City, Osaka, Japan.
Osaka University · JPKindai University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cyclin G-associated kinase (GAK), a key player in clathrin-mediated membrane trafficking, is overexpressed in various cancer cells. Here, we report that GAK expression is positively correlated with the Gleason score in surgical specimens from prostate cancer patients. Embryonic fibroblasts from knockout mice expressing a kinase-dead (KD) form of GAK showed constitutive hyper-phosphorylation of the epidermal growth factor receptor (EGFR). In addition to the well-known EGFR inhibitors gefitinib and erlotinib, the dietary flavonoid luteolin was a potent inhibitor of the Ser/Thr kinase activity of GAK in vitro. Co-administration of luteolin and gefitinib to PC-3 cells had a greater effect on cell viability than administration of either compound alone; this decrease in viability was associated with drastic down-regulation of GAK protein expression. A comprehensive microRNA array analysis revealed increased expression of miR-630 and miR-5703 following treatment of PC-3 cells with luteolin and/or gefitinib, and exogenous overexpression of miR-630 caused growth arrest of these cells. GAK appears to be essential for cell death because co-administration of gefitinib and luteolin to EGFR-deficient U2OS osteosarcoma cells also had a greater effect on cell viability than administration of either compound alone. Taken together, these findings suggest that GAK may be a new therapeutic target for prostate cancer and osteosarcoma.

Indexed as

Active Transport, Cell NucleusAntineoplastic AgentsApoptosisCell Cycle CheckpointsCell Line, TumorCell ProliferationCell SurvivalErbB ReceptorsGefitinibGene ExpressionGene Expression Regulation, NeoplasticHumansIntracellular Signaling Peptides and ProteinsLuteolinMaleMicroRNAsAntineoplastic AgentsErbB ReceptorsGAK protein, humanGefitinibIntracellular Signaling Peptides and ProteinsLuteolinMicroRNAsMIRN630 microRNA, humanProtein Kinase InhibitorsProtein Serine-Threonine KinasesQuinazolines

Identifiers

PMID24971999
PMCPMC4074034
OpenAlexW2067037955

What OpenQuestion holds

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LicenceCC BY
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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.