Evidence map›Paper›PMID 24448324›Full record

ArticleCancer biology & therapy2014

Loss of GATA3 in bladder cancer promotes cell migration and invasion.

Yi Li, Hitoshi Ishiguro, Takashi Kawahara, Eiji Kashiwagi, Koji Izumi, Hiroshi Miyamoto

Open access · bronzeAbstract read
In one paragraph

Article in Cancer biology & therapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 15% 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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 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

6 authors at 4 institutions in 2 countries.

Yi LiDepartment of Pathology and Laboratory Medicine; University of Rochester Medical Center; Rochester, NY USA; Department of Urology; 2nd Affiliated Hospital; Zhejiang University School of Medicine; Hangzhou, PR China.
Hitoshi IshiguroDepartment of Pathology and Laboratory Medicine; University of Rochester Medical Center; Rochester, NY USA; Departments of Pathology and Urology; Johns hopkins University school of Medicine; Baltimore, MD UsA.
Takashi KawaharaDepartment of Pathology and Laboratory Medicine; University of Rochester Medical Center; Rochester, NY USA; Departments 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.
Koji IzumiDepartment of Pathology and Laboratory Medicine; University of Rochester Medical Center; Rochester, NY USA.
Hiroshi MiyamotoDepartment of Pathology and Laboratory Medicine; University of Rochester Medical Center; Rochester, NY USA; Departments of Pathology and Urology; Johns hopkins University school of Medicine; Baltimore, MD UsA.
Johns Hopkins University · USUniversity of Rochester Medical Center · USJohns Hopkins Medicine · USZhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The transcription factor GATA3 is known as a breast tumor suppressor as well as a urothelial marker, and its loss is often seen in high-grade invasive bladder cancer. Nonetheless, GATA3 functions in bladder cancer cells remain largely unknown. In this study, we assessed the effects of GATA3 silencing via RNA interference on cell migration, invasion, and proliferation of bladder cancer. GATA3 expression was downregulated in all four bladder cancer lines examined, compared with a non-neoplastic urothelial line SVHUC. Knockdown of GATA3 in the bladder cancer lines (5637, TCC-SUP, J82) resulted in promotion of cell migration and invasion as well as increases in the expression of their related molecules, such as vascular endothelial growth factor, matrix metalloproteinase (MMP)-2, and MMP-9, and the activity of MMP-2 and MMP-9. GATA3 loss was also associated with an increasing level of a mesenchymal marker N-cadherin and a decreasing level of an epithelial marker β-catenin. Consistent with these findings, enforced expression of GATA3 in UMUC3 inhibited cell migration and invasion. However, GATA3 showed marginal effects on bladder cancer cell viability and the expression of cell cycle- or apoptosis-related molecules. Additionally, in contrast to bladder cancer lines, no significant effects of GATA3 silencing on cell migration were seen in SVHUC. These findings suggest that GATA3 plays an important role in the prevention of bladder cancer progression and metastasis by inhibiting cell migration and invasion as well as epithelial-to-mesenchymal transition.

Indexed as

Cell MovementCell LineCell Line, TumorCell ProliferationGATA3 Transcription FactorHumansNeoplasm InvasivenessUrinary Bladder NeoplasmsGATA3 Transcription Factorbladder cancercell invasioncell migrationcell proliferationGATA3

Identifiers

PMID24448324
PMCPMC3979820
OpenAlexW2069100816

What OpenQuestion holds

Textmetadata
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.