Evidence map›Paper›PMID 41806200›Full record

ArticleJournal of gastroenterology2026

Extracellular vesicle-encapsulated microRNA-425 promotes tumor development and serves as a biomarker for pancreatic ductal adenocarcinoma.

Kazuya Koyama, Kenji Takahashi, Yusuke Ono, Kyohei Oyama, Nobue Tamamura, Hiroki Tanaka, Fumi Asai, Yukino Kobayashi, Chiho Maeda, Yu Ohtaki and 13 more

Abstract read
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In one paragraph

Article in Journal of gastroenterology, 2026. 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

23 authors.

Kazuya KoyamaDivision of Gastroenterology, Department of Medicine, Asahikawa Medical University, 2-1-1-1, Midorigaoka Higashi, Asahikawa, Hokkaido, 078-8510, Japan.
Kenji TakahashiDivision of Gastroenterology, Department of Medicine, Asahikawa Medical University, 2-1-1-1, Midorigaoka Higashi, Asahikawa, Hokkaido, 078-8510, Japan. t-kenji@asahikawa-med.ac.jp.ORCID 0000-0002-6166-6848
Yusuke OnoDivision of Gastroenterology, Department of Medicine, Asahikawa Medical University, 2-1-1-1, Midorigaoka Higashi, Asahikawa, Hokkaido, 078-8510, Japan.
Kyohei OyamaDepartment of Cardiac Surgery, Asahikawa Medical University, Asahikawa, Hokkaido, Japan.
Nobue TamamuraDivision of Gastroenterology, Department of Medicine, Asahikawa Medical University, 2-1-1-1, Midorigaoka Higashi, Asahikawa, Hokkaido, 078-8510, Japan.
Hiroki TanakaDivision of Tumor Pathology, Department of Pathology, Asahikawa Medical University, Asahikawa, Hokkaido, Japan.
Fumi AsaiH.U. Group Research Institute G.K., Akiruno, Tokyo, Japan.
Yukino KobayashiDepartment of Pharmacology, Asahikawa Medical University, Asahikawa, Hokkaido, Japan.
Chiho MaedaInstitute of Biomedical Research, Sapporo Higashi Tokushukai Hospital, Sapporo, Hokkaido, Japan.
Yu OhtakiDivision of Gastroenterology, Department of Medicine, Asahikawa Medical University, 2-1-1-1, Midorigaoka Higashi, Asahikawa, Hokkaido, 078-8510, Japan.
Hiroki SatoDivision of Gastroenterology, Department of Medicine, Asahikawa Medical University, 2-1-1-1, Midorigaoka Higashi, Asahikawa, Hokkaido, 078-8510, Japan.
Tetsuhiro OkadaDivision of Gastroenterology, Department of Medicine, Asahikawa Medical University, 2-1-1-1, Midorigaoka Higashi, Asahikawa, Hokkaido, 078-8510, Japan.
Hidemasa KawabataDivision of Gastroenterology, Department of Medicine, Asahikawa Medical University, 2-1-1-1, Midorigaoka Higashi, Asahikawa, Hokkaido, 078-8510, Japan.
Hidetaka IwamotoDivision of Gastroenterology, Department of Medicine, Asahikawa Medical University, 2-1-1-1, Midorigaoka Higashi, Asahikawa, Hokkaido, 078-8510, Japan.
Yohei KitanoDivision of Gastroenterology, Department of Medicine, Asahikawa Medical University, 2-1-1-1, Midorigaoka Higashi, Asahikawa, Hokkaido, 078-8510, Japan.
Taito ItohCenter for Intractable Diseases and ImmunoGenomics, National Institutes of Biomedical Innovation, Health and Nutrition, Osaka, Japan.
Akiko MatsudaDepartment of Gastroenterology, Faculty of Medicine, Yamagata University, Yamagata, Japan.
Tatsutoshi InuzukaH.U. Group Research Institute G.K., Akiruno, Tokyo, Japan.
Kenzui TaniueDivision of Gastroenterology, Department of Medicine, Asahikawa Medical University, 2-1-1-1, Midorigaoka Higashi, Asahikawa, Hokkaido, 078-8510, Japan.
Koh NakayamaDepartment of Pharmacology, Asahikawa Medical University, Asahikawa, Hokkaido, Japan.
Mikihiro FujiyaDivision of Gastroenterology, Department of Medicine, Asahikawa Medical University, 2-1-1-1, Midorigaoka Higashi, Asahikawa, Hokkaido, 078-8510, Japan.
Toshikatsu OkumuraDivision of Gastroenterology, Department of Medicine, Asahikawa Medical University, 2-1-1-1, Midorigaoka Higashi, Asahikawa, Hokkaido, 078-8510, Japan.
Yusuke MizukamiDivision of Gastroenterology, Department of Medicine, Asahikawa Medical University, 2-1-1-1, Midorigaoka Higashi, Asahikawa, Hokkaido, 078-8510, Japan.

Funding

Japan Society for the Promotion of Science 21K07954Japan Society for the Promotion of Science 22KK0125Japan Society for the Promotion of Science 24K02431
6 · The paper itself

Abstract

backgroundMicroRNAs (miRNAs) enclosed within extracellular vesicles (EVs) have emerged as crucial players in carcinogenesis and are increasingly recognized as potential cancer biomarkers. However, their significance in pancreatic ductal adenocarcinoma (PDAC) and their utility for early detection remain unclear.

methodsWe utilized microarray analysis to identify the miRNAs highly expressed in PDAC cells compared to immortalized pancreatic ductal cells. Functional studies investigated the effect of miRNA overexpression and inhibition on PDAC cells invasion/migration and associated signaling pathways. Additionally, we examined the transfer of miRNA via EVs and their potential impact on the recipient PDAC cells. Serum samples from 30 healthy individuals, 30 patients with intraductal papillary mucinous neoplasm, and 30 PDAC were analyzed for EV miRNA expression using digital PCR.

resultsMiR-425 emerged as an oncogenic miRNA upregulated in PDAC, suppressing phosphatase and tensin homolog (PTEN) while activating phosphatidylinositol 3-kinase (PI3K)/Akt and epithelial-to-mesenchymal transition (EMT) pathways. Treatment with miR-425-enriched EVs induced EMT in PDAC cells by suppressing PTEN, enhancing invasion and migration. Serum EV miR-425 levels tended to be higher in PDAC patients, particularly in Stage I/II compared to Stage III/IV, although the difference was not statistically significant. Combining EV miR-425 with CA19-9 improved diagnostic performance over CA19-9 alone, achieving a sensitivity 93%, specificity 91%, and AUC of 0.98.

conclusionOur finding suggested the role of intercellular transfer of EV miR-425 in inducing EMT via PTEN/PI3K/Akt pathway modulation, thereby promoting invasion and migration of PDAC cells. Serum EV miR-425 holds promise as a potential biomarker for early diagnosis of PDAC.

Indexed as

Biomarkers, TumorCarcinoma, Pancreatic DuctalExtracellular VesiclesMicroRNAsPancreatic NeoplasmsAgedCell Line, TumorCell MovementEarly Detection of CancerEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHumansMaleMiddle AgedNeoplasm InvasivenessBiomarkers, TumorMicroRNAsMIRN425 microRNA, humanPTEN PhosphohydrolasePTEN protein, humanEMTExtracellular vesiclesLiquid biopsyMicroRNAPancreatic ductal adenocarcinoma

Identifiers

PMID41806200

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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.