Evidence map›Paper›PMID 31193165›Full record

ArticleBiochemistry and biophysics reports2019

E-cadherin loss in RMG-1 cells inhibits cell migration and its regulation by Rho GTPases.

Misako Haraguchi, Tomoko Fukushige, Takuro Kanekura, Masayuki Ozawa

Open access · goldAbstract read
In one paragraph

Article in Biochemistry and biophysics reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

9 citing papers in PubMed, 15 citations in OpenAlex.

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  9. EMT signaling: potential contribution of CRISPR/Cas gene editing.Cellular and molecular life sciences : CMLS · 2020
    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

4 authors at 1 institution in 1 country.

Misako HaraguchiDepartment of Biochemistry and Molecular Biology, Japan.
Tomoko FukushigeDermatology of Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima, Japan.
Takuro KanekuraDermatology of Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima, Japan.
Masayuki OzawaLaboratory for Cell Adhesion and Tissue Patterning, RIKEN Center for Developmental Biology. Kobe, Japan.
Kagoshima University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

E-cadherin is an adherens junction protein that forms intercellular contacts in epithelial cells. Downregulation of E-cadherin is frequently observed in epithelial tumors and it is a hallmark of epithelial-mesenchymal transition (EMT). However, recent findings suggest that E-cadherin plays a more complex role in certain types of cancers. Previous studies investigating the role of E-cadherin mainly used gene-knockdown systems; therefore, we used the CRISPR/Cas9n system to develop E-cadherin-knockout (EcadKO) ovarian cancer RMG-1 cell to clarify the role of E-cadherin in RMG-1 cells. EcadKO RMG-1 cells demonstrated a complete loss of the adherens junctions and failed to form cell clusters. Cell-extracellular matrix (ECM) interactions were increased in EcadKO RMG-1 cells. Upregulation of integrin beta1 and downregulation of collagen 4 were confirmed. EcadKO RMG-1 cells showed decreased β-catenin levels and decreased expression of its transcriptional target cyclin D1. Surprisingly, a marked decrease in the migratory ability of EcadKO RMG-1 cells was observed and the cellular response to Rho GTPase inhibitors was diminished. Thus, we demonstrated that E-cadherin in RMG-1 cells is indispensable for β-catenin expression and β-catenin mediated transcription and Rho GTPase-regulated directionally persistent cell migration.

Indexed as

Cell migrationCRISPR/Cas9nDispaseE-cadherinRhoGTPseβ-catenin

Identifiers

PMID31193165
PMCPMC6520553
OpenAlexW2944922746

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.