Evidence map›Paper›PMID 24914344›Full record

ArticleWorld journal of gastroenterology2014

Down-regulated γ-catenin expression is associated with tumor aggressiveness in esophageal cancer.

Wang-Kai Fang, Lian-Di Liao, Wei Gu, Bo Chen, Zhi-Yong Wu, Jian-Yi Wu, Jian Shen, Li-Yan Xu, En-Min Li

Open access · hybridAbstract read
In one paragraph

Article in World journal of gastroenterology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

13 citing papers in PubMed, 18 citations in OpenAlex.

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  13. Desmosome regulation and signaling in disease.Cell and tissue research · 2015
    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

9 authors at 1 institution in 1 country.

Wang-Kai FangWang-Kai Fang, Wei Gu, Jian-Yi Wu, En-Min Li, Department of Biochemistry and Molecular Biology, The Key Laboratory of Molecular Biology for High Cancer Incidence Coastal Chaoshan Area, Shantou University Medical College, Shantou 515041, Guangdong Province, China.
Lian-Di LiaoWang-Kai Fang, Wei Gu, Jian-Yi Wu, En-Min Li, Department of Biochemistry and Molecular Biology, The Key Laboratory of Molecular Biology for High Cancer Incidence Coastal Chaoshan Area, Shantou University Medical College, Shantou 515041, Guangdong Province, China.
Wei GuWang-Kai Fang, Wei Gu, Jian-Yi Wu, En-Min Li, Department of Biochemistry and Molecular Biology, The Key Laboratory of Molecular Biology for High Cancer Incidence Coastal Chaoshan Area, Shantou University Medical College, Shantou 515041, Guangdong Province, China.
Bo ChenWang-Kai Fang, Wei Gu, Jian-Yi Wu, En-Min Li, Department of Biochemistry and Molecular Biology, The Key Laboratory of Molecular Biology for High Cancer Incidence Coastal Chaoshan Area, Shantou University Medical College, Shantou 515041, Guangdong Province, China.
Zhi-Yong WuWang-Kai Fang, Wei Gu, Jian-Yi Wu, En-Min Li, Department of Biochemistry and Molecular Biology, The Key Laboratory of Molecular Biology for High Cancer Incidence Coastal Chaoshan Area, Shantou University Medical College, Shantou 515041, Guangdong Province, China.
Jian-Yi WuWang-Kai Fang, Wei Gu, Jian-Yi Wu, En-Min Li, Department of Biochemistry and Molecular Biology, The Key Laboratory of Molecular Biology for High Cancer Incidence Coastal Chaoshan Area, Shantou University Medical College, Shantou 515041, Guangdong Province, China.
Jian ShenWang-Kai Fang, Wei Gu, Jian-Yi Wu, En-Min Li, Department of Biochemistry and Molecular Biology, The Key Laboratory of Molecular Biology for High Cancer Incidence Coastal Chaoshan Area, Shantou University Medical College, Shantou 515041, Guangdong Province, China.
Li-Yan XuWang-Kai Fang, Wei Gu, Jian-Yi Wu, En-Min Li, Department of Biochemistry and Molecular Biology, The Key Laboratory of Molecular Biology for High Cancer Incidence Coastal Chaoshan Area, Shantou University Medical College, Shantou 515041, Guangdong Province, China.
En-Min LiWang-Kai Fang, Wei Gu, Jian-Yi Wu, En-Min Li, Department of Biochemistry and Molecular Biology, The Key Laboratory of Molecular Biology for High Cancer Incidence Coastal Chaoshan Area, Shantou University Medical College, Shantou 515041, Guangdong Province, China.
MRC Laboratory of Molecular Biology · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimTo evaluate the significance of γ-catenin in clinical pathology, cellular function and signaling mechanism in esophageal squamous cell carcinoma (ESCC).

methodsThe mRNA expression of γ-catenin was detected by real-time quantitative reverse transcription-polymerase chain reaction in 95 tissue specimens and evaluated for association with the clinicopathologic characteristics and survival time of patients with ESCC. siRNAs against human γ-catenin were used to inhibit γ-catenin expression. Hanging drop aggregation assay and dispase-based dissociation assay were performed to detect the effect of γ-catenin on ESCC cell-cell adhesion. Transwell assay was performed to determine cell migration. Luciferase-based transcriptional reporter assay (TOPflash) was used to measure β-catenin-dependent transcription in cells with reduced γ-catenin expression. The expression and subcellular localizations of β-catenin and E-cadherin were examined using Western blot and immunofluorescence analysis.

resultsγ-catenin mRNA expression was significantly associated with tumor histological grade (P = 0.017) in ESCC. Kaplan-Meier survival analysis showed that γ-catenin expression levels had an impact on the survival curve, with low γ-catenin indicating worse survival (P = 0.003). The multivariate Cox regression analysis demonstrated that γ-catenin was an independent prognostic factor for survival. Experimentally, silencing γ-catenin caused defects in cell-cell adhesion and a concomitant increase in cell migration in both KYSE150 and TE3 ESCC cells. Analysis of Wnt signaling revealed no activation event associated with γ-catenin expression. Total β-catenin and Triton X-100-insoluble β-catenin were significantly reduced in the γ-catenin-specific siRNA-transfected KYSE150 and TE3 cells, whereas Triton X-100-soluble β-catenin was not altered. Moreover, knocking down γ-catenin expression resulted in a significant decrease of E-cadherin and Triton X-100-insoluble desmocollin-2, along with reduced β-catenin and E-cadherin membrane localization in ESCC cells.

conclusionγ-catenin is a tumor suppressor in ESCC and may serve as a prognostic marker. Dysregulated expression of γ-catenin may play important roles in ESCC progression.

Indexed as

Gene Expression Regulation, NeoplasticAdultAgedAged, 80 and overCarcinoma, Squamous CellCell AdhesionCell MovementDesmocollinsDesmoplakinsDisease ProgressionEsophageal NeoplasmsFemalegamma CateninGene SilencingHumansKaplan-Meier EstimateDesmocollinsDesmoplakinsDSC2 protein, humangamma CateninJUP protein, humanRNA, MessengerRNA, Small InterferingCell-cell adhesionCell migrationEsophageal squamous cell carcinomaIndependent prognostic factorγ-catenin

Identifiers

PMID24914344
PMCPMC4024793
OpenAlexW2034346294

What OpenQuestion holds

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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.