Evidence map›Paper›PMID 31336560›Full record

ArticleInternational journal of molecular sciences2019

Cell Type-Specific TGF-β Mediated EMT in 3D and 2D Models and Its Reversal by TGF-β Receptor Kinase Inhibitor in Ovarian Cancer Cell Lines.

Wafa Al Ameri, Ikhlak Ahmed, Fatima M Al-Dasim, Yasmin Ali Mohamoud, Iman K Al-Azwani, Joel A Malek, Thasni Karedath

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 16% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

  1. Pooled it
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  13. SFPQ Promotes Lung Cancer MalignancyFrontiers in oncology · 2022
    Article
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  17. Role of the lysyl oxidase family in organ development (Review).Experimental and therapeutic medicine · 2020
    Review
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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 1 institution in 1 country.

Wafa Al AmeriDepartment of Genetic Medicine, Weill Cornell Medicine-Qatar, Education City, Qatar Foundation, Doha P.O. Box No. 24144, Qatar.
Ikhlak AhmedDepartment of Genetic Medicine, Weill Cornell Medicine-Qatar, Education City, Qatar Foundation, Doha P.O. Box No. 24144, Qatar.
Fatima M Al-DasimDepartment of Genetic Medicine, Weill Cornell Medicine-Qatar, Education City, Qatar Foundation, Doha P.O. Box No. 24144, Qatar.
Yasmin Ali MohamoudGenomics Core, Weill Cornell Medicine-Qatar, Education City, Qatar Foundation, Doha, Qatar.
Iman K Al-AzwaniSidra Medicine, Doha P.O. Box No. 26999, Qatar.
Joel A MalekDepartment of Genetic Medicine, Weill Cornell Medicine-Qatar, Education City, Qatar Foundation, Doha P.O. Box No. 24144, Qatar.
Thasni KaredathDepartment of Genetic Medicine, Weill Cornell Medicine-Qatar, Education City, Qatar Foundation, Doha P.O. Box No. 24144, Qatar. tka2001@qatar-med.cornell.edu.ORCID 0000-0001-5482-5954
Weill Cornell Medical College in Qatar · QA

Funding

Qatar Foundation BMRP
6 · The paper itself

Abstract

Transcriptome profiling of 3D models compared to 2D models in various cancer cell lines shows differential expression of TGF-β-mediated and cell adhesion pathways. Presence of TGF-β in these cell lines shows an increased invasion potential which is specific to cell type. In the present study, we identified exogenous addition of TGF-β can induce Epithelial to Mesenchymal Transition (EMT) in a few cancer cell lines. RNA sequencing and real time PCR were carried out in different ovarian cancer cell lines to identify molecular profiling and metabolic profiling. Since EMT induction by TGF-β is cell-type specific, we decided to select two promising ovarian cancer cell lines as model systems to study EMT. TGF-β modulation in EMT and cancer invasion were successfully depicted in both 2D and 3D models of SKOV3 and CAOV3 cell lines. Functional evaluation in 3D and 2D models demonstrates that the addition of the exogenous TGF-β can induce EMT and invasion in cancer cells by turning them into aggressive phenotypes. TGF-β receptor kinase I inhibitor (LY364947) can revert the TGF-β effect in these cells. In a nutshell, TGF-β can induce EMT and migration, increase aggressiveness, increase cell survival, alter cell characteristics, remodel the Extracellular Matrix (ECM) and increase cell metabolism favorable for tumor invasion and metastasis. We concluded that transcriptomic and phenotypic effect of TGF-β and its inhibitor is cell-type specific and not cancer specific.

Indexed as

Adenosine TriphosphateCell Line, TumorCell MovementEpithelial-Mesenchymal TransitionExtracellular MatrixFemaleHumansOvarian NeoplasmsProtein Kinase InhibitorsReceptors, Transforming Growth Factor betaSignal TransductionTransforming Growth Factor betaTumor Cells, CulturedAdenosine TriphosphateProtein Kinase InhibitorsReceptors, Transforming Growth Factor betaTransforming Growth Factor beta3D modelsEMTovarian cancerSKOV3TGF-β

Identifiers

PMID31336560
PMCPMC6678358
OpenAlexW2963364055

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.