Evidence map›Paper›PMID 29247567›Full record

ArticleCancer science2018

ADAM9 is over-expressed in human ovarian clear cell carcinomas and suppresses cisplatin-induced cell death.

Mari Ueno, Takayuki Shiomi, Satsuki Mochizuki, Miyuki Chijiiwa, Masayuki Shimoda, Yae Kanai, Fumio Kataoka, Akira Hirasawa, Nobuyuki Susumu, Daisuke Aoki and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 17% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.

  1. Pooled it
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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 1 institution in 1 country.

Mari UenoDepartment of Pathology, Keio University School of Medicine, Tokyo, Japan.
Takayuki ShiomiDepartment of Pathology, Keio University School of Medicine, Tokyo, Japan.
Satsuki MochizukiDepartment of Pathology, Keio University School of Medicine, Tokyo, Japan.
Miyuki ChijiiwaDepartment of Pathology, Keio University School of Medicine, Tokyo, Japan.
Masayuki ShimodaDepartment of Pathology, Keio University School of Medicine, Tokyo, Japan.
Yae KanaiDepartment of Pathology, Keio University School of Medicine, Tokyo, Japan.
Fumio KataokaDepartment of Obstetrics and Gynecology, Keio University School of Medicine, Tokyo, Japan.
Akira HirasawaDepartment of Obstetrics and Gynecology, Keio University School of Medicine, Tokyo, Japan.
Nobuyuki SusumuDepartment of Obstetrics and Gynecology, Keio University School of Medicine, Tokyo, Japan.
Daisuke AokiDepartment of Obstetrics and Gynecology, Keio University School of Medicine, Tokyo, Japan.
Yasunori OkadaDepartment of Pathology, Keio University School of Medicine, Tokyo, Japan.ORCID http://orcid.org/0000-0001-9208-4755
Keio University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

ADAMs (a disintegrin and metalloproteinases) are involved in various biological events such as cell adhesion, migration and invasion, membrane protein shedding and proteolysis. However, there have been no systematic studies on the expression of ADAMs in human ovarian carcinomas. We therefore examined mRNA expression of all the proteolytic ADAM species including ADAM8, 9, 10, 12, 15, 17, 19, 20, 21, 28, 30, 33 and ADAMDEC1 in human ovarian carcinomas, and found that prototype membrane-anchored ADAM9m, but not secreted isoform ADAM9s, is significantly over-expressed in carcinomas than in control non-neoplastic ovarian tissue. Among the histological subtypes of serous, endometrioid, mucinous and clear cell carcinomas, ADAM9m expression was highest in clear cell carcinomas. Immunohistochemistry showed that all the clear cell carcinoma samples displayed ADAM9m primarily on the carcinoma cell membrane. By immunoblotting, ADAM9m was detected mainly in an active form in the clear cell carcinoma tissues. When two clear cell carcinoma cell lines (RMG-I and TOV21G cells) with ADAM9m expression were treated with cisplatin, viability was significantly reduced and apoptosis increased in ADAM9m knockdown cells compared with mock transfectants. In addition, treatment of the cells with neutralizing anti-ADAM9m antibody significantly decreased viability compared with non-immune IgG, whereas ADAM9m over-expression significantly increased viability compared with mock transfectants. Our data show, to the best of our knowledge, for the first time, that ADAM9m is over-expressed in an activated form in human ovarian clear cell carcinomas, and suggest that ADAM9m plays a key role in cisplatin resistance.

Indexed as

Drug Resistance, NeoplasmADAM ProteinsAdenocarcinoma, Clear CellAntineoplastic AgentsApoptosisCell Line, TumorCell MovementCisplatinFemaleGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansMembrane ProteinsOvarian NeoplasmsUp-RegulationADAM9 protein, humanADAM ProteinsAntineoplastic AgentsCisplatinMembrane Proteinsa disintegrin and metalloproteinase 9chemoresistancecisplatinclear cell carcinomaovarian carcinoma

Identifiers

PMID29247567
PMCPMC5797829
OpenAlexW2773046739

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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.