Evidence map›Paper›PMID 26497678›Full record

ArticleOncotarget2016

Therapeutic potential of targeting cell division cycle associated 5 for oral squamous cell carcinoma.

Norihiko Tokuzen, Koh-ichi Nakashiro, Hiroshi Tanaka, Kazuki Iwamoto, Hiroyuki Hamakawa

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 22% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.

  1. Pooled it
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  12. Cyclin-Dependent Kinase 1 (CDK1) is Co-Expressed with CDCA5: Their Functions in Gastric Cancer Cell Line MGC-803.Medical science monitor : international medical journal of experimental and clinical research · 2020
    Article
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  14. Analysis of the Expression ofBioMed research international · 2020
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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

5 authors at 1 institution in 1 country.

Norihiko TokuzenDepartment of Oral and Maxillofacial Surgery, Ehime University Graduate School of Medicine, Shitsukawa, Toon, Ehime, Japan.
Koh-ichi NakashiroDepartment of Oral and Maxillofacial Surgery, Ehime University Graduate School of Medicine, Shitsukawa, Toon, Ehime, Japan.
Hiroshi TanakaDepartment of Oral and Maxillofacial Surgery, Ehime University Graduate School of Medicine, Shitsukawa, Toon, Ehime, Japan.
Kazuki IwamotoDepartment of Oral and Maxillofacial Surgery, Ehime University Graduate School of Medicine, Shitsukawa, Toon, Ehime, Japan.
Hiroyuki HamakawaDepartment of Oral and Maxillofacial Surgery, Ehime University Graduate School of Medicine, Shitsukawa, Toon, Ehime, Japan.
Ehime University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Molecularly targeted drugs are used in the treatment of a variety of malignant tumors, but this approach to developing novel therapies for oral squamous cell carcinoma (OSCC) has lagged behind the progress seen for other cancers. We have attempted to find appropriate molecular targets for OSCC and identified cell division cycle associated 5 (CDCA5) as a cancer-related gene which was overexpressed in all the human OSCC cells tested by microarray analysis. In this study, we investigated the expression and function of CDCA5 in OSCC. First, we confirmed that CDCA5 was overexpressed in 4 human OSCC cell lines by quantitative RT-PCR and Western blotting. We then tested the effect of synthetic small interfering RNAs specific for CDCA5 on the growth and invasion of human OSCC cells. Knockdown of CDCA5 markedly inhibited the growth of OSCC cells in vitro and in vivo. We also examined the expression of CDCA5 protein in 80 cases of OSCC immunohistochemically and found a significant association between CDCA5 expression levels and overall survival. These results suggest that CDCA5 functions as a critical gene supporting OSCC progression and that targeting CDCA5 may be a useful therapeutic strategy for OSCC.

Indexed as

Adaptor Proteins, Signal TransducingAged, 80 and overAnimalsCarcinoma, Squamous CellCell CycleCell Cycle ProteinsCell Line, TumorCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansMaleMiceMice, NudeMiddle AgedMouth NeoplasmsAdaptor Proteins, Signal TransducingCDCA5 protein, humanCell Cycle ProteinsRNA, Small Interferingcell cyclecell division cycle associated 5 (CDCA5)molecular targeted therapyoral squamous cell carcinoma (OSCC)prognosis

Identifiers

PMID26497678
PMCPMC4823039
OpenAlexW1866578610

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.