Evidence map›Paper›PMID 23517130›Full record

ArticleBMC cancer2013

Targeting Id1 reduces proliferation and invasion in aggressive human salivary gland cancer cells.

Tomoki Sumida, Ryuichi Murase, Akiko Onishi-Ishikawa, Sean D McAllister, Hiroyuki Hamakawa, Pierre-Yves Desprez

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

8 citing papers in PubMed, 14 citations in OpenAlex.

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  8. A review: Immunological markers for malignant salivary gland tumors.Journal of oral biology and craniofacial research
    Review
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

6 authors at 3 institutions in 2 countries.

Tomoki SumidaDepartment of Oral and Maxillofacial Surgery, Ehime University School of Medicine, 454 Shitsukawa, Toon-City, Ehime 791-0295, Japan. tomoki@m.ehime-u.ac.jp
Ryuichi Murase
Akiko Onishi-Ishikawa
Sean D McAllister
Hiroyuki Hamakawa
Pierre-Yves Desprez
Ehime University · JPCalifornia Pacific Medical Center · USCancer Research Institute · US

Funding

Cannabinoids Control Breast Cancer Progression Through Id-1R01CA135281 · NCI · CALIFORNIA PACIFIC MED CTR RES INSTITUTE · PI MCALLISTER, SEAN D · 2009 to 2012
$1.4M
ID-1 EXPRESSION IN BREAST EPITHELIAL CELLSR01CA082548 · NCI · CALIFORNIA PACIFIC MED CTR RES INSTITUTE · PI DESPREZ, PIERRE-YVES · 1999 to 2002
$644k
NCI NIH HHS CA082548NCI NIH HHS CA135281
6 · The paper itself

Abstract

backgroundSalivary gland cancer (SGC) is one of the common malignancies of the head and neck area. It develops in the minor and major salivary glands and sometimes metastasizes to other organs, particularly to the lungs. Inhibitors of differentiation (Id) proteins are negative regulators of basic helix-loop-helix transcription factors that control malignant cell behavior and tumor aggressiveness in many tissues. In this study, our goal was to determine the potential role of Id proteins, particularly Id1, during human SGC cell progression.

methodsWe first determined the expression levels of Id1 and Id2 in four SGC cell lines: two adenocarcinoma of the salivary gland (HSG and HSY) and two adenoid cystic carcinoma (ACC2 and ACCM) cell lines. We then used constructs that expressed antisense cDNAs to Id1 or Id2 to knockdown the expression of these proteins in cell lines where they were highly expressed, and determined the effects of the knockdown on cell proliferation, migration and invasion.

resultsId1 mRNA and protein were detectable in all cell lines, and expression of Id2 was variable, from absent to high. The ACC2 and ACCM cell lines expressed both Id1 and Id2, but Id1 was expressed at a higher level in the more aggressive ACCM cell line in comparison to ACC2 cells as confirmed by Id1 promoter-reporter assays. We therefore focused on the ACCM cells for the remainder of the study. We found that proliferation and invasiveness of ACCM cells were strongly reduced after Id1 knockdown whereas Id2 suppression had only a slight effect. Results of scratch and colony formation assays also confirmed that ACCM cell aggressiveness was significantly reduced upon Id1 knockdown. Finally, this knockdown resulted in reduced c-myc and enhanced cyclin-dependent kinase inhibitor p21 expression.

conclusionsThese results demonstrate that Id1 plays an important role in the control of human SGC cell aggressiveness and suggest a potential role as a marker of diagnosis, prognosis and progression of SGCs. Id1 suppression could represent a novel and effective approach for the treatment of salivary gland cancer.

Indexed as

AdenocarcinomaCarcinoma, Adenoid CysticCell Line, TumorCell MovementCell ProliferationCyclin-Dependent Kinase Inhibitor p21Down-RegulationGene Knockdown TechniquesHumansInhibitor of Differentiation Protein 1Inhibitor of Differentiation Protein 2Proto-Oncogene Proteins c-mycSalivary Gland NeoplasmsTumor Stem Cell AssayUp-RegulationCyclin-Dependent Kinase Inhibitor p21Inhibitor of Differentiation Protein 1Inhibitor of Differentiation Protein 2Proto-Oncogene Proteins c-myc

Identifiers

PMID23517130
PMCPMC3639030
OpenAlexW2138344590

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.