Evidence map›Paper›PMID 32366234›Full record

ArticleBMC cancer2020

FAT4 silencing promotes epithelial-to-mesenchymal transition and invasion via regulation of YAP and β-catenin activity in ovarian cancer.

Shika Hanif Malgundkar, Ikram Burney, Mansour Al Moundhri, Moza Al Kalbani, Ritu Lakhtakia, Aikou Okamoto, Yahya Tamimi

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.0field-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

17 citing papers in PubMed, 24 citations in OpenAlex.

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  10. The Clinical Significance of Genetic Variation in Ovarian Cancer.International journal of molecular sciences · 2023
    Article
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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

7 authors at 3 institutions in 3 countries.

Shika Hanif MalgundkarDepartments of Biochemistry, Obstetrics & Gynecology, College of Medicine and Health Sciences, Sultan Qaboos University, PO Box 35, PC 123, Muscat, Sultanate of Oman.
Ikram BurneyDepartments ofMedicine, and Obstetrics & Gynecology, College of Medicine and Health Sciences, Sultan Qaboos University, PO Box 35, PC 123, Muscat, Sultanate of Oman.
Mansour Al MoundhriDepartments ofMedicine, and Obstetrics & Gynecology, College of Medicine and Health Sciences, Sultan Qaboos University, PO Box 35, PC 123, Muscat, Sultanate of Oman.
Moza Al KalbaniObstetrics & Gynecology, College of Medicine and Health Sciences, Sultan Qaboos University, PO Box 35, PC 123, Muscat, Sultanate of Oman.
Ritu LakhtakiaDepartment of Pathology, College of Medicine, Mohammed Bin Rashid University of Medicine and Health Sciences, Dubai, UAE.
Aikou OkamotoDepartment of Obstetrics and Gynecology, The Jikei University School of Medicine, Tokyo, Japan.
Yahya TamimiDepartments of Biochemistry, Obstetrics & Gynecology, College of Medicine and Health Sciences, Sultan Qaboos University, PO Box 35, PC 123, Muscat, Sultanate of Oman. yahyatam@squ.edu.om.ORCID http://orcid.org/0000-0002-5469-789X
Sultan Qaboos University · OMJikei University School of Medicine · JPMohammed Bin Rashid University of Medicine and Health Sciences · AE

Funding

His Majesty's Trust Fund (HMTF) SR/MED/BIOC/14/01
6 · The paper itself

Abstract

backgroundThe adhesion molecule, FAT4, has a tumor suppressor function with a critical role in the epithelial-to-mesenchymal-transition (EMT) and anti-malignant growth in several cancers. No study has investigated yet its role in epithelial ovarian cancer (EOC) progression. In the present study, we examined the role of FAT4 in proliferation and metastasis, and its mechanisms of interaction in these processes.

methodsWe have performed cell viability, colony formation, and invasion assays in ovarian cancer cells treated with siRNA to knockdown FAT4 gene expression. The regulatory effects of FAT4 on proteins involved in apoptotic, Wnt, Hippo, and retinoblastoma signaling pathways were evaluated by Western blotting following FAT4 repression. Also, 426 ovarian tumor samples and 88 non-tumor samples from the Gene Expression Profiling Interactive Analysis (GEPIA) database were analyzed for the expression of FAT4. Pearson's correlation was performed to determine the correlation between FAT4 and the E2F5, cyclin D1, cdk4, and caspase 9 expressions.

resultsLower expression of FAT4 was observed in ovarian cancer cell lines and human samples as compared to non-malignant tissues. This down-regulation seems to enhance cell viability, invasion, and colony formation. Silencing FAT4 resulted in the upregulation of E2F5, vimentin, YAP, β-catenin, cyclin D1, cdk4, and Bcl2, and in the downregulation of GSK-3-β, and caspase 9 when compared to control. Furthermore, regulatory effects of FAT4 on the EMT and aggressive phenotype seem to occur through Hippo, Wnt, and cell cycle pathways.

conclusionFAT4 downregulation promotes increased growth and invasion through the activation of Hippo and Wnt-β-catenin pathways.

Indexed as

Epithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticAdaptor Proteins, Signal Transducingbeta CateninCadherinsCell Line, TumorCell MovementCell ProliferationE2F5 Transcription FactorFemaleGene Knockdown TechniquesGenes, Tumor SuppressorHumansOvarian NeoplasmsSignal TransductionTranscription FactorsAdaptor Proteins, Signal Transducingbeta CateninCadherinsCTNNB1 protein, humanE2F5 protein, humanE2F5 Transcription FactorFAT4 protein, humanTranscription FactorsTumor Suppressor ProteinsYAP1 protein, humanYAP-Signaling ProteinsFAT4InvasionOvarian cancerSilencingYAP

Identifiers

PMID32366234
PMCPMC7197128
OpenAlexW3021426086

What OpenQuestion holds

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LicenceCC BY
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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.