Evidence map›Paper›PMID 25638160›Full record

ArticleOncotarget2015

Cyclosporine A and tacrolimus inhibit bladder cancer growth through down-regulation of NFATc1.

Takashi Kawahara, Eiji Kashiwagi, Hiroki Ide, Yi Li, Yichun Zheng, Yurina Miyamoto, George J Netto, Hitoshi Ishiguro, Hiroshi Miyamoto

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
5.3field-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

43 citing papers in PubMed, 67 citations in OpenAlex.

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  8. Calcineurin-mediated dephosphorylation stabilizes E2F1 protein by suppressing binding of the FBXW7 ubiquitin ligase subunit.Proceedings of the National Academy of Sciences of the United States of America · 2024
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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

9 authors at 3 institutions in 1 country.

Takashi KawaharaDepartments of Pathology and Urology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Eiji KashiwagiDepartments of Pathology and Urology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Hiroki IdeDepartments of Pathology and Urology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Yi LiDepartment of Pathology and Laboratory Medicine, University of Rochester Medical Center, Rochester, NY, USA.
Yichun ZhengDepartments of Pathology and Urology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Yurina MiyamotoDepartment of Pathology and Laboratory Medicine, University of Rochester Medical Center, Rochester, NY, USA.
George J NettoDepartments of Pathology and Urology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Hitoshi IshiguroDepartments of Pathology and Urology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Hiroshi MiyamotoDepartments of Pathology and Urology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
University of Rochester Medical Center · USJohns Hopkins Medicine · USJohns Hopkins University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The functional role of nuclear factor of activated T-cells (NFAT), a key regulator of the immune response, in bladder cancer progression remains uncertain. In this study, we assessed biological significance of NFAT in human bladder cancer. Immunohistochemistry detected nuclear/cytoplasmic NFATc1 signals in 14 (21.5%)/34 (52.3%), respectively, of 65 muscle-invasive bladder carcinomas and showed that patients with nuclear NFATc1-positive tumor had a significantly higher risk of disease progression (P = 0.006). In bladder cancer cell lines, cyclosporine A (CsA) and tacrolimus (FK506), immunosuppressant drugs/non-selective NFAT inhibitors, attenuated NFATc1 expression and its nuclear translocation, NFAT transcriptional activity, and the expression of cyclooxygenase-2 and c-myc, downstream targets of NFATc1. NFAT inhibition via NFATc1-small interfering RNA (siRNA) or treatment with these NFAT inhibitors resulted in decreases in cell viability/colony formation, cell migration/invasion, and the expression/activity of MMP-2 and MMP-9, as well as an increase in apoptosis, in the parental/control lines. No significant additional inhibition in the viability and invasion of NFATc1-siRNA cells was seen. In xenograft-bearing mice, CsA and FK506 significantly retarded tumor growth. These results suggest that NFATc1 plays an important role in bladder cancer outgrowth. Thus, NFATc1 inactivation, especially using CsA and FK506, has the potential of being a therapeutic approach for bladder cancer.

Indexed as

AnimalsAntineoplastic Combined Chemotherapy ProtocolsCell Line, TumorCyclosporineDown-RegulationHumansMaleMiceMice, Inbred NODMice, SCIDNFATC Transcription FactorsTacrolimusUrinary Bladder NeoplasmsXenograft Model Antitumor AssaysCyclosporineNFATC1 protein, humanNFATC Transcription FactorsTacrolimus

Identifiers

PMID25638160
PMCPMC4359316
OpenAlexW1581371393

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.