Evidence map›Paper›PMID 39661112›Full record

ArticleJournal of gastroenterology2025

Serum Mac2-binding protein glycosylated isomer (M2BPGi) as a prognostic biomarker in pancreatic ductal adenocarcinoma: iCAFs-derived M2BPGi drives tumor invasion.

Naotaka Kugiyama, Katsuya Nagaoka, Rin Yamada, Takehisa Watanabe, Hajime Yamazaki, Shinya Ushijima, Fumiya Otsuka, Yukiko Uramoto, Hajime Iwasaki, Motohiro Yoshinari and 5 more

Abstract read
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In one paragraph

Article in Journal of gastroenterology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
  2. Review
  3. 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

15 authors.

Naotaka KugiyamaDepartment of Gastroenterology and Hepatology, Faculty of Life Sciences, Kumamoto University, 1-1-1 Honjo, Chuo-ku, Kumamoto-shi, Kumamoto, 860-0811, Japan.
Katsuya NagaokaDepartment of Gastroenterology and Hepatology, Faculty of Life Sciences, Kumamoto University, 1-1-1 Honjo, Chuo-ku, Kumamoto-shi, Kumamoto, 860-0811, Japan.
Rin YamadaDepartment of Cell Pathology, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.
Takehisa WatanabeDepartment of Gastroenterology and Hepatology, Faculty of Life Sciences, Kumamoto University, 1-1-1 Honjo, Chuo-ku, Kumamoto-shi, Kumamoto, 860-0811, Japan.
Hajime YamazakiSection of Clinical Epidemiology, Department of Community Medicine, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Shinya UshijimaDepartment of Gastroenterology and Hepatology, Faculty of Life Sciences, Kumamoto University, 1-1-1 Honjo, Chuo-ku, Kumamoto-shi, Kumamoto, 860-0811, Japan.
Fumiya OtsukaDepartment of Gastroenterology and Hepatology, Faculty of Life Sciences, Kumamoto University, 1-1-1 Honjo, Chuo-ku, Kumamoto-shi, Kumamoto, 860-0811, Japan.
Yukiko UramotoDepartment of Gastroenterology and Hepatology, Faculty of Life Sciences, Kumamoto University, 1-1-1 Honjo, Chuo-ku, Kumamoto-shi, Kumamoto, 860-0811, Japan.
Hajime IwasakiDepartment of Gastroenterology and Hepatology, Faculty of Life Sciences, Kumamoto University, 1-1-1 Honjo, Chuo-ku, Kumamoto-shi, Kumamoto, 860-0811, Japan.
Motohiro YoshinariDepartment of Gastroenterology and Hepatology, Faculty of Life Sciences, Kumamoto University, 1-1-1 Honjo, Chuo-ku, Kumamoto-shi, Kumamoto, 860-0811, Japan.
Shunpei HashigoDepartment of Gastroenterology and Hepatology, Kumamoto City Hospital, Kumamoto, Japan.
Hiromitsu HayashiDepartment of Gastroenterological Surgery, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.
Takatsugu IshimotoDepartment of Gastroenterological Surgery, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.
Yoshihiro KomoharaDepartment of Cell Pathology, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.
Yasuhito TanakaDepartment of Gastroenterology and Hepatology, Faculty of Life Sciences, Kumamoto University, 1-1-1 Honjo, Chuo-ku, Kumamoto-shi, Kumamoto, 860-0811, Japan. ytanaka@kumamoto-u.ac.jp.ORCID 0000-0002-2473-6966

Funding

Japan Agency for Medical Research and Development AMED JP24fk0210103h0003JSPS KAKENHI 22K15971
6 · The paper itself

Abstract

backgroundPancreatic ductal adenocarcinoma (PDAC) is an aggressive malignancy with a poor prognosis. Mac2-binding protein glycosylated isomer (M2BPGi), a known biomarker for liver fibrosis, is also elevated in other fibrotic tissues. However, its role in PDAC remains unexplored. This study investigates the potential of M2BPGi as a prognostic biomarker for PDAC and elucidates its role in cancer progression.

methodsWe analyzed serum M2BPGi levels in 83 PDAC patients and 60 healthy controls, examining the relationship with clinical outcomes. Tissue immunostaining and in vitro experiments were conducted to investigate M2BPGi-secreting cells and its role.

resultsSerum M2BPGi levels were significantly higher in PDAC patients than in controls (0.98 vs. 0.59, p < 0.0001). Notably, elevated serum M2BPGi was associated with worse progression-free survival (144 days vs. 260 days, p = 0.017) and overall survival (OS) (245 days vs. 541 days, p < 0.001) following chemotherapy. Multivariable Cox regression analysis further confirmed that a high serum M2BPGi level is an independent risk factor for OS (HR: 2.44, 95% CI 1.26-4.74, p = 0.008). Immunostaining revealed that M2BPGi is secreted by both cancer cells and cancer-associated fibroblasts (CAFs), with high M2BP expression in CAFs correlating with poor prognosis. Furthermore, M2BPGi-secreting CAFs exhibited characteristics of inflammatory CAFs. M2BPGi directly activated mTOR signaling and epithelial-mesenchymal transition in PDAC cells, enhancing their invasive and migratory capabilities.

conclusionsOur findings identify M2BPGi as a promising prognostic biomarker for PDAC. Moreover, we demonstrate that inflammatory CAFs promote tumor invasion and contribute to poor outcomes by secreting M2BPGi, revealing a novel mechanism of PDAC progression.

Indexed as

Antigens, NeoplasmBiomarkers, TumorCarcinoma, Pancreatic DuctalPancreatic NeoplasmsAgedCancer-Associated FibroblastsCase-Control StudiesDisease ProgressionFemaleHumansMaleMembrane GlycoproteinsMiddle AgedNeoplasm InvasivenessPrognosisAntigens, NeoplasmBiomarkers, TumorMembrane GlycoproteinsTAA90K protein, humanBiomarkerCAFsM2BPGiPancreatic ductal adenocarcinomaTumor microenvironment

Identifiers

PMID39661112

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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.