Evidence map›Paper›PMID 36982569›Full record

ReviewInternational journal of molecular sciences2023

Claudin-4: A New Molecular Target for Epithelial Cancer Therapy.

Rina Fujiwara-Tani, Shiori Mori, Ruiko Ogata, Rika Sasaki, Ayaka Ikemoto, Shingo Kishi, Masuo Kondoh, Hiroki Kuniyasu

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

29 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
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  15. Review
  16. Article
  17. Article
  18. Claudins in Cancer: A Current and Future Therapeutic Target.International journal of molecular sciences · 2024
    Review
  19. Review
  20. 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

8 authors at 2 institutions in 1 country.

Rina Fujiwara-TaniDepartment of Molecular Pathology, Nara Medical University, Kashihara 634-8521, Japan.
Shiori MoriDepartment of Molecular Pathology, Nara Medical University, Kashihara 634-8521, Japan.
Ruiko OgataDepartment of Molecular Pathology, Nara Medical University, Kashihara 634-8521, Japan.
Rika SasakiDepartment of Molecular Pathology, Nara Medical University, Kashihara 634-8521, Japan.
Ayaka IkemotoDepartment of Molecular Pathology, Nara Medical University, Kashihara 634-8521, Japan.
Shingo KishiDepartment of Molecular Pathology, Nara Medical University, Kashihara 634-8521, Japan.
Masuo KondohDrug Innovation Center, Graduate School of Pharmaceutical Sciences, Osaka University, 6-1 Yamadaoka, Suita 565-0871, Japan.
Hiroki KuniyasuDepartment of Molecular Pathology, Nara Medical University, Kashihara 634-8521, Japan.ORCID 0000-0003-2298-8825
Nara Medical University · JPThe University of Osaka · JP

Funding

Ministry of Education, Culture, Sports, Science and Technology 19K16564Ministry of Education, Culture, Sports, Science and Technology 20K21659Ministry of Education, Culture, Sports, Science and Technology 21K10143
6 · The paper itself

Abstract

Claudin-4 (CLDN4) is a key component of tight junctions (TJs) in epithelial cells. CLDN4 is overexpressed in many epithelial malignancies and correlates with cancer progression. Changes in CLDN4 expression have been associated with epigenetic factors (such as hypomethylation of promoter DNA), inflammation associated with infection and cytokines, and growth factor signaling. CLDN4 helps to maintain the tumor microenvironment by forming TJs and acts as a barrier to the entry of anticancer drugs into tumors. Decreased expression of CLDN4 is a potential marker of epithelial-mesenchymal transition (EMT), and decreased epithelial differentiation due to reduced CLDN4 activity is involved in EMT induction. Non-TJ CLDN4 also activates integrin beta 1 and YAP to promote proliferation, EMT, and stemness. These roles in cancer have led to investigations of molecular therapies targeting CLDN4 using anti-CLDN4 extracellular domain antibodies, gene knockdown, clostridium perfringens enterotoxin (CPE), and C-terminus domain of CPE (C-CPE), which have demonstrated the experimental efficacy of this approach. CLDN4 is strongly involved in promoting malignant phenotypes in many epithelial cancers and is regarded as a promising molecular therapeutic target.

Indexed as

Antineoplastic AgentsNeoplasmsCell Line, TumorClaudin-3Claudin-4EnterotoxinsEpithelial CellsSignal TransductionTight JunctionsAntineoplastic AgentsClaudin-3Claudin-4Enterotoxinscancerclaudin-4molecular targetnon-tight junction claudintight junction

Identifiers

PMID36982569
PMCPMC10051602
OpenAlexW4324149030

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.