Evidence map›Paper›PMID 34385585›Full record

ArticleScientific reports2021

EMID1, a multifunctional molecule identified in a murine model for the invasion independent metastasis pathway.

Takuya Kawata, Koji Muramatsu, Namiko Shishito, Naoki Ichikawa-Tomikawa, Takuma Oishi, Yuko Kakuda, Yasuto Akiyama, Ken Yamaguchi, Michiie Sakamoto, Takashi Sugino

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.0field-weighted citation impact, top 23% 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

7 citing papers in PubMed, 6 citations in OpenAlex.

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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

10 authors at 4 institutions in 1 country.

Takuya KawataDivision of Pathology, Shizuoka Cancer Center, Shizuoka, 411-8777, Japan.
Koji MuramatsuDivision of Pathology, Shizuoka Cancer Center, Shizuoka, 411-8777, Japan.
Namiko ShishitoDepartment of Cardiology, Southern TOHOKU General Hospital, Koriyama, Japan.
Naoki Ichikawa-TomikawaDepartment of Basic Pathology, Fukushima Medical University School of Medicine, Fukushima, Japan.
Takuma OishiDivision of Pathology, Shizuoka Cancer Center, Shizuoka, 411-8777, Japan.
Yuko KakudaDivision of Pathology, Shizuoka Cancer Center, Shizuoka, 411-8777, Japan.
Yasuto AkiyamaDivision of Immunotherapy, Shizuoka Cancer Center Research Institute, Shizuoka, Japan.
Ken YamaguchiShizuoka Cancer Center Hospital and Research Institute, Shizuoka, Japan.
Michiie SakamotoDepartment of Pathology, Keio University School of Medicine, Tokyo, Japan.
Takashi SuginoDivision of Pathology, Shizuoka Cancer Center, Shizuoka, 411-8777, Japan. t.sugino@scchr.jp.
Shizuoka Cancer Center · JPKeio University · JPFukushima Medical University · JPSouthern Tohoku General Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

EMI Domain Containing 1 (EMID1) was identified as a potential candidate metastasis-promoting gene. We sought to clarify the molecular function of EMID1 and the protein expression. Overexpression and knockdown studies using mouse tumor cell lines identified two novel functions of EMID1: intracellular signaling involving enhancement of cell growth via cell cycle promotion and suppression of cell motility, and inhibition of cell-matrix adhesion by extracellularly secreted EMID1. EMID1 deposited on the culture dish induced self-detachment of cells that overexpressed the protein and inhibited adhesion of additionally seeded cells. This multifunctional property involving both intracellular signaling and the extracellular matrix suggests that EMID1 may be a matricellular proteins. Expression analysis using immunohistochemical staining revealed expression of EMID1 that was limited to chief cells of the gastric fundic gland and β cells of the pancreatic islets in normal adult human tissues, implying cell-specific functions of this molecule. In addition, increased expression of EMID1 protein detected in some cases of human cancers implies that EMID1 might be a new therapeutic target for cancer treatment.

Indexed as

AnimalsCell AdhesionCell Line, TumorCell MovementCell ProliferationDisease Models, AnimalExtracellular MatrixGastric FundusGene Expression Regulation, NeoplasticHumansInsulin-Secreting CellsMiceNeoplasm InvasivenessNeoplasm MetastasisNeoplastic ProcessesSignal Transduction

Identifiers

PMID34385585
PMCPMC8361151
OpenAlexW3192473769

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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.