Evidence map›Paper›PMID 41365610›Full record

ArticleCancer medicine2025

Plexin Domain Containing 2, a Protein Specifically Expressed and Elevated in Human Pancreatic Cancer Tissue and Serum, Influences Cell Proliferation by Correlating With Cortactin.

Junya Tsuboi, Akiko Eguchi, Hiroyuki Inoue, Masako Ichishi, Masatomo Go, Ryo Okajima, Noriko Yasuhara, Ryo Nakagawa, Mina Tempaku, Kiyora Izuoka and 13 more

Abstract read
In one paragraph

Article in Cancer medicine, 2025. 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
–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

2 citing papers in PubMed.

  1. Review
  2. 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

23 authors.

Junya TsuboiDepartment of Gastroenterology and Hepatology, Mie University Graduate School of Medicine, Tsu, Japan.
Akiko EguchiDepartment of Gastroenterology and Hepatology, Mie University Graduate School of Medicine, Tsu, Japan.ORCID https://orcid.org/0000-0002-0555-2707
Hiroyuki InoueDepartment of Gastroenterology and Hepatology, Mie University Graduate School of Medicine, Tsu, Japan.
Masako IchishiDepartment of Oncologic Pathology, Mie University Graduate School of Medicine, Tsu, Japan.
Masatomo GoDepartment of Physical Chemistry, School of Pharmacy and Pharmaceutical Sciences, Hoshi University, Shinagawa, Japan.
Ryo OkajimaDepartment of Physical Chemistry, School of Pharmacy and Pharmaceutical Sciences, Hoshi University, Shinagawa, Japan.
Noriko YasuharaDepartment of Life Science College of Humanities and Science, Nihon University, Chiyoda, Japan.
Ryo NakagawaOmiya City Clinic, Saitama, Japan.
Mina TempakuDepartment of Gastroenterology and Hepatology, Mie University Graduate School of Medicine, Tsu, Japan.
Kiyora IzuokaDepartment of Gastroenterology and Hepatology, Mie University Graduate School of Medicine, Tsu, Japan.
Takamitsu TanakaDepartment of Gastroenterology and Hepatology, Mie University Graduate School of Medicine, Tsu, Japan.
Kenji NoseDepartment of Gastroenterology and Hepatology, Mie University Graduate School of Medicine, Tsu, Japan.
Naohiko YoshizawaDepartment of Gastroenterology and Hepatology, Mie University Graduate School of Medicine, Tsu, Japan.
Yoshifumi HirokawaDepartment of Oncologic Pathology, Mie University Graduate School of Medicine, Tsu, Japan.
Reiko YamadaDepartment of Gastroenterology and Hepatology, Mie University Graduate School of Medicine, Tsu, Japan.
Kyosuke TanakaDepartment of Gastroenterology and Hepatology, Mie University Graduate School of Medicine, Tsu, Japan.ORCID https://orcid.org/0000-0002-1402-7832
Takeshi KawamuraIsotope Science Center, The University of Tokyo, Bunkyō, Japan.
Tetsuji YamaguchiDepartment of Health Promotion and Preventive Medicine, Mie University Graduate School of Medicine, Tsu, Japan.
Yoshiyuki TakeiDepartment of Gastroenterology and Hepatology, Mie University Graduate School of Medicine, Tsu, Japan.
Motoh IwasaDepartment of Gastroenterology and Hepatology, Mie University Graduate School of Medicine, Tsu, Japan.
Takefumi YamashitaDepartment of Physical Chemistry, School of Pharmacy and Pharmaceutical Sciences, Hoshi University, Shinagawa, Japan.
Masatoshi WatanabeDepartment of Oncologic Pathology, Mie University Graduate School of Medicine, Tsu, Japan.
Hayato NakagawaDepartment of Gastroenterology and Hepatology, Mie University Graduate School of Medicine, Tsu, Japan.

Funding

Japan Society for the Promotion of Science 22K07982
6 · The paper itself

Abstract

backgroundPancreatic ductal adenocarcinoma (PDAC) is a highly aggressive cancer with limited treatment options. Plexin domain containing 2 (PLXDC2), a tumor endothelial marker, has been implicated in several cancers, but its role in PDAC remains unclear. This study aimed to investigate the role of PLXDC2 and its interaction with cortactin in PDAC.

methodPLXDC2 and cortactin expression levels were assessed by immunohistochemistry in human PDAC tissues. Serum PLXDC2 levels were measured using ELISA. PDAC cell lines were transfected with PLXDC2 siRNA. The effects of PLXDC2 knockdown on cortactin and oncogene expression, as well as cell proliferation, were evaluated using quantitative PCR, Western blotting, immunofluorescence, and proliferation assays. Computational modeling with AlphaFold3 predicted the 3D structure of the PLXDC2-cortactin complex and designed inhibitory peptide.

resultsPLXDC2 was overexpressed in PDAC tissues and serum, with an AUROC of 0.987 compared to healthy individuals. PLXDC2 co-expressed with cortactin in human PDAC tissues. In PDAC cells, PLXDC2 knockdown led to decreased cortactin expression, followed by a reduction of oncogene (c-myc and Oct4) expression and proliferation. Computational analysis predicted that the SH3 domain of cortactin binds to the PSI domain of PLXDC2. Peptide-mediated inhibition of the PLXDC2-cortactin binding, by targeting the SH3 domain of cortactin, led to a reduction of oncogenic and proliferative genes.

conclusionsPLXDC2 is a potential biomarker of PDAC diagnosis. Targeting the PLXDC2-cortactin interaction may offer a novel therapeutic strategy.

Indexed as

Carcinoma, Pancreatic DuctalCortactinNerve Tissue ProteinsPancreatic NeoplasmsAgedBiomarkers, TumorCell Line, TumorCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansMaleMiddle AgedBiomarkers, TumorCortactinCTTN protein, humanNerve Tissue ProteinsAlphaFold3biomarkercortactinpancreatic adenocarcinomaplexin domain containing 2therapeutic target

Identifiers

PMID41365610
PMCPMC12688484

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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.