Evidence map›Paper›PMID 24386490›Full record

Trial reportPloS one2013

Kinesin family member 4A: a potential predictor for progression of human oral cancer.

Yasuyuki Minakawa, Atsushi Kasamatsu, Hirofumi Koike, Morihiro Higo, Dai Nakashima, Yukinao Kouzu, Yosuke Sakamoto, Katsunori Ogawara, Masashi Shiiba, Hideki Tanzawa and 1 more

Open access · goldAbstract readClinical Trial
In one paragraph

Trial report in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 14% 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

47 citing papers in PubMed, 1 synthesis or guideline pooled it, 107 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

11 authors at 2 institutions in 1 country.

Yasuyuki MinakawaDepartment of Clinical Molecular Biology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chiba, Japan.
Atsushi KasamatsuDepartment of Dentistry and Oral-Maxillofacial Surgery, Chiba University Hospital, 1-8-1 Inohana, Chiba, Japan.
Hirofumi KoikeDepartment of Dentistry and Oral-Maxillofacial Surgery, Chiba University Hospital, 1-8-1 Inohana, Chiba, Japan.
Morihiro HigoDepartment of Dentistry and Oral-Maxillofacial Surgery, Chiba University Hospital, 1-8-1 Inohana, Chiba, Japan.
Dai NakashimaDepartment of Clinical Molecular Biology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chiba, Japan.
Yukinao KouzuDepartment of Dentistry and Oral-Maxillofacial Surgery, Chiba University Hospital, 1-8-1 Inohana, Chiba, Japan.
Yosuke SakamotoDepartment of Dentistry and Oral-Maxillofacial Surgery, Chiba University Hospital, 1-8-1 Inohana, Chiba, Japan.
Katsunori OgawaraDepartment of Dentistry and Oral-Maxillofacial Surgery, Chiba University Hospital, 1-8-1 Inohana, Chiba, Japan.
Masashi ShiibaDepartment of Medical Oncology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chiba, Japan.
Hideki TanzawaDepartment of Clinical Molecular Biology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chiba, Japan ; Department of Dentistry and Oral-Maxillofacial Surgery, Chiba University Hospital, 1-8-1 Inohana, Chiba, Japan.
Katsuhiro UzawaDepartment of Clinical Molecular Biology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chiba, Japan ; Department of Dentistry and Oral-Maxillofacial Surgery, Chiba University Hospital, 1-8-1 Inohana, Chiba, Japan.
Chiba University Hospital · JPChiba University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundKinesin family member 4A (KIF4A), a microtubule-based motor protein, was implicated in regulation of chromosomal structure and kinetochore microtubule dynamics. Considering the functions of KIF4A, we assumed that KIF4A is involved in progression of oral squamous cell carcinomas (OSCCs) via activation of the spindle assembly checkpoint (SAC). However, little is known about the relevance of KIF4A in the behavior of OSCC. We investigated the KIF4A expression status and its functional mechanisms in OSCC.

methodsThe KIF4A expression levels in seven OSCC-derived cells were analyzed by quantitative reverse transcriptase-polymerase chain reaction and immunoblotting analyses. Using a KIF4A knockdown model, we assessed the expression of (SAC)-related molecules (BUB1, MAD2, CDC20, and cyclin B1), cell-cycle, and cellular proliferation. In addition to in vitro data, the clinical correlation between the KIF4A expression levels in primary OSCCs (n = 106 patients) and the clinicopathologic status by immunohistochemistry (IHC) also were evaluated.

resultsKIF4A mRNA and protein were up-regulated significantly (P < 0.05) in seven OSCC-derived cells compared with human normal oral keratinocytes. In the KIF4A knockdown cells, SAC activation was observed via increased BUB1 expression on the kinetochores, appropriate kinetochore localization of MAD2, down-regulation of CDC20, up-regulation of cyclin B1, and cell-cycle arrested at G2/M phase. The results showed that cellular proliferation of KIF4A knockdown cells decreased significantly (P < 0.05) compared with control cells. IHC showed that KIF4A expression in primary OSCCs was significantly (P < 0.05) greater than in the normal oral counterparts and that KIF4A-positive OSCCs were correlated closely (P < 0.05) with tumoral size.

conclusionsOur results proposed for the first time that KIF4A controls cellular proliferation via SAC activation. Therefore, KIF4A might be a key regulator for tumoral progression in OSCCs.

Indexed as

G2 Phase Cell Cycle CheckpointsGene Expression Regulation, NeoplasticCarcinoma, Squamous CellCell Line, TumorFemaleHumansKinesinsMaleMouth NeoplasmsNeoplasm ProteinsUp-RegulationKIF4A protein, humanKinesinsNeoplasm Proteins

Identifiers

PMID24386490
PMCPMC3875575
OpenAlexW2012031864

What OpenQuestion holds

Textmetadata
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.