Evidence map›Paper›PMID 30881495›Full record

ArticleOncology letters2019

Silencing of

Yoshinori Inagaki, Tomohiko Tokunaga, Mitsuru Yanai, Dan Wu, Jiyi Huang, Hiroki Nagase, Noboru Fukuda, Toshinori Ozaki, Masayoshi Soma, Kyoko Fujiwara

Open access · diamondAbstract read
In one paragraph

Article in Oncology letters, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.3field-weighted citation impact, top 48% 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

2 citing papers in PubMed, 4 citations in OpenAlex.

  1. Review
  2. The Roles of EphB2 in Cancer.Frontiers in cell and developmental biology · 2022
    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

10 authors at 2 institutions in 1 country.

Yoshinori InagakiDivision of General Medicine, Department of Medicine, Nihon University School of Medicine, Itabashi, Tokyo 173-8610, Japan.
Tomohiko TokunagaDivision of General Medicine, Department of Medicine, Nihon University School of Medicine, Itabashi, Tokyo 173-8610, Japan.
Mitsuru YanaiDivision of General Medicine, Department of Medicine, Nihon University School of Medicine, Itabashi, Tokyo 173-8610, Japan.
Dan WuDepartment of Oncology, The 5th Hospital of Xiamen, Xiamen, Fujian 361101, P.R. China.
Jiyi HuangDepartment of Nephropathy, The 5th Hospital of Xiamen, Xiamen, Fujian 361101, P.R. China.
Hiroki NagaseLaboratory of Cancer Genetics, Chiba Cancer Center Research Institute, Chiba 260-8717, Japan.
Noboru FukudaDivision of Nephrology, Hypertension and Endocrinology, Department of Medicine, Nihon University School of Medicine, Itabashi, Tokyo 173-8610, Japan.
Toshinori OzakiDepartment of DNA Damage Signaling, Research Center, The 5th Hospital of Xiamen, Xiamen, Fujian 361101, P.R. China.
Masayoshi SomaDivision of General Medicine, Department of Medicine, Nihon University School of Medicine, Itabashi, Tokyo 173-8610, Japan.
Kyoko FujiwaraDivision of General Medicine, Department of Medicine, Nihon University School of Medicine, Itabashi, Tokyo 173-8610, Japan.
Nihon University · JPChiba Cancer Center · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Erythropoietin-producing hepatocellular (Eph) receptors and their ligand ephrins serve crucial roles in the interactions among epithelial cells. Eph receptor/ephrin signaling regulates cell functions, including proliferation, differentiation and migration, via these cell-cell interactions. We reported previously that EPHB2, a member of the Eph receptor family, was highly expressed in chemically induced cutaneous squamous cell carcinoma (cSCC) tissues in mice. Although the higher expression level of EPHB2 has been observed in various human cancers, its roles in the development and progression of cancers are still unclear. In the present study, the functional implications of EPHB2 in the acquisition of malignant phenotypes of cSCC cells was investigated. Silencing of EPHB2 in the human cSCC cell line A431 induced epithelial-mesenchymal transition (EMT)-like morphological changes accompanied by a significant upregulation of epithelial-mesenchymal transition-associated genes such as zinc finger E-box binding homeobox 1/2. In addition, silencing of EPHB2 suppressed anchorage-independent cell growth under 3D culture conditions. Consistent with these observations, EPHB2 exhibited higher levels of expression in tumor spheres formed under 3D culture conditions than in cells cultured in adherent form, and the expression pattern of EMT markers indicated that EMT was suppressed in tumor spheres. The results of the present study indicated that EPHB2 serves a pivotal role in promoting the anchorage-independent growth of A431 cells through the suppression of EMT.

Indexed as

anchorage-independent cell growthepithelial-mesenchymal transitionerythropoietin-producing hepatocellular B2skin squamous cell carcinoma

Identifiers

PMID30881495
PMCPMC6403506
OpenAlexW2914028472

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.