Evidence map›Paper›PMID 40361399›Full record

ArticleCancers2025

The Role of Claudin-1 in Enhancing Pancreatic Cancer Aggressiveness and Drug Resistance via Metabolic Pathway Modulation.

Daisuke Kyuno, Hinae Asano, Reona Okumura, Kumi Takasawa, Akira Takasawa, Takumi Konno, Yuna Nakamori, Kazufumi Magara, Yusuke Ono, Masafumi Imamura and 3 more

Abstract read
In one paragraph

Article in Cancers, 2025. 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
–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

7 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Article
  5. MUC13-Associated Molecular Interactome in Pancreatic Cancer.Computational and structural biotechnology journal · 2026
    Article
  6. Article
  7. 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

13 authors.

Daisuke KyunoDepartment of Pathology, Sapporo Medical University School of Medicine, Sapporo 060-8556, Japan.ORCID 0000-0003-4672-535X
Hinae AsanoDepartment of Pathology, Sapporo Medical University School of Medicine, Sapporo 060-8556, Japan.
Reona OkumuraDepartment of Pathology, Sapporo Medical University School of Medicine, Sapporo 060-8556, Japan.
Kumi TakasawaDivision of Tumor Pathology, Department of Pathology, Asahikawa Medical University, Asahikawa 078-8510, Japan.
Akira TakasawaDivision of Tumor Pathology, Department of Pathology, Asahikawa Medical University, Asahikawa 078-8510, Japan.
Takumi KonnoDepartment of Cell Science, Institute of Cancer Research, Sapporo Medical University School of Medicine, Sapporo 060-8556, Japan.ORCID 0000-0002-9339-3864
Yuna NakamoriDepartment of Pathology, Sapporo Medical University School of Medicine, Sapporo 060-8556, Japan.
Kazufumi MagaraDepartment of Pathology, Sapporo Medical University School of Medicine, Sapporo 060-8556, Japan.
Yusuke OnoDepartment of Pathology, Sapporo Medical University School of Medicine, Sapporo 060-8556, Japan.
Masafumi ImamuraDepartment of Surgery, Division of Gastroenterological Surgery, Sapporo Medical University, Sapporo 060-8556, Japan.ORCID 0000-0001-7669-7666
Yasutoshi KimuraDepartment of Surgery, Division of Gastroenterological Surgery, Sapporo Medical University, Sapporo 060-8556, Japan.
Takashi KojimaDepartment of Cell Science, Institute of Cancer Research, Sapporo Medical University School of Medicine, Sapporo 060-8556, Japan.ORCID 0000-0002-6346-4588
Makoto OsanaiDepartment of Pathology, Sapporo Medical University School of Medicine, Sapporo 060-8556, Japan.

Funding

Japan Society for the Promotion of Science JP21K08715Japan Society for the Promotion of Science JP24K11826Wellcome Trust 202212
6 · The paper itself

Abstract

BACKGROUND/

objectivesPancreatic ductal adenocarcinoma is a lethal malignancy, necessitating an understanding of its molecular mechanisms for the development of new therapeutic strategies. The tight junction protein claudin-1, known to influence cellular functions in various cancers and is considered a therapeutic target, remains unclear in pancreatic cancer.

methodsThis study assessed claudin-1 expression in resected pancreatic cancer samples, public databases, and pancreatic cancer cell lines.

resultsClaudin-1 was markedly overexpressed in pancreatic ductal adenocarcinoma and intraepithelial neoplasia compared to normal ducts, and high claudin-1 levels were an independent predictor of poor prognosis.

conclusionsThese findings indicate that the abnormal expression of claudin-1 promotes tumor progression and drug resistance through its interaction with aldo-keto reductase proteins, highlighting claudin-1 and aldo-keto reductase family proteins as potential biomarkers and therapeutic targets for pancreatic cancer.

Indexed as

aldo-keto reductasechemoresistanceclaudin-1pancreatic cancertight junction

Identifiers

PMID40361399
PMCPMC12070999

What Socratic 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 Socratic graph.