Evidence map›Paper›PMID 38825958›Full record

ArticleTissue barriers2025

The roles of tight junction protein cingulin in human endometrioid endometrial cancer.

Arisa Kura, Kimihito Saito, Takumi Konno, Takayuki Kohno, Hiroshi Shimada, Tadahi Okada, Soshi Nishida, Daichi Ishii, Motoki Matsuura, Tsuyoshi Saito and 1 more

Abstract read
In one paragraph

Article in Tissue barriers, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Article
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

11 authors.

Arisa KuraDepartment of Obstetrics and Gynecology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Kimihito SaitoDepartment of Obstetrics and Gynecology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Takumi KonnoDepartment of Cell Science, Institute of Cancer Research, Sapporo Medical University School of Medicine, Sapporo, Japan.
Takayuki KohnoDepartment of Cell Science, Institute of Cancer Research, Sapporo Medical University School of Medicine, Sapporo, Japan.
Hiroshi ShimadaDepartment of Obstetrics and Gynecology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Tadahi OkadaDepartment of Obstetrics and Gynecology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Soshi NishidaDepartment of Otolaryngology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Daichi IshiiDepartment of Thoracic Surgery, Sapporo Medical University School of Medicine, Sapporo, Japan.
Motoki MatsuuraDepartment of Obstetrics and Gynecology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Tsuyoshi SaitoDepartment of Obstetrics and Gynecology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Takashi KojimaDepartment of Cell Science, Institute of Cancer Research, Sapporo Medical University School of Medicine, Sapporo, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The bicellular tight junction molecule cingulin (CGN) binds to microtubules in centrosomes. Furthermore, CGN contributes to the tricellular tight junction (tTJ) proteins lipolysis-stimulated lipoprotein receptor (LSR) and tricellulin (TRIC). CGN as well as LSR decreased during the malignancy of endometrioid endometrial cancer (EEC). Although tTJ protein LSR is involved in the malignancy of some cancers, including EEC, the role of CGN is unknown. In this study, we investigated the roles of CGN with tTJ proteins in human EEC cells by using the CGN-overexpressing EEC cell line Sawano. In 2D cultures, CGN was colocalized with LSR and TRIC at tTJ or at γ-tubulin-positive centrosomes. In immunoprecipitation with CGN antibodies, CGN directly bound to LSR, TRIC, and β-tubulin. Knockdown of CGN by the siRNA decreased the epithelial barrier and enhanced cell proliferation, migration and invasion, as well as knockdown of LSR. In the Sawano cells cocultured with normal human endometrial stromal cells, knockdown of CGN decreased expression of LSR and TRIC via MAPK and AMPK pathways. In 2.5D cultures, knockdown of CGN induced the formation of abnormal cysts and increased the permeability of FD-4 to the lumen. In 2D and 2.5D cultures, treatment with β-estradiol with or without EGF or TGF-β decreased CGN expression and the epithelial permeability barrier and enhanced cell migration, and pretreatment with EW7197+AG1478, U0126 or an anti-IL-6 antibody prevented this. In conclusion, CGN, with tTJ proteins might suppress the malignancy of human EEC and its complex proteins are sensitive to estrogen and growth factors derived from stromal cells.

Indexed as

Carcinoma, EndometrioidEndometrial NeoplasmsTight JunctionsCell Line, TumorFemaleHumansCGNepithelial permeability barrierestrogenhuman endometrioid endometrial cancerLSRmalignancyTRICtricellular tight junction

Identifiers

PMID38825958
PMCPMC12363535

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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.