Evidence map›Paper›PMID 41039587›Full record

ArticleCell communication and signaling : CCS2025

IGFBP2 alteration contributes to prostate cancer progression by modulating prostate stroma activation.

Mingguo Huang, Shintaro Narita, Hiromi Sato, Yuya Sekine, Mizuki Kobayashi, Soki Kashima, Ryohei Yamamoto, Atsushi Koizumi, Taketoshi Nara, Kazuyuki Numakura and 4 more

Abstract read
In one paragraph

Article in Cell communication and signaling : CCS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

14 authors.

Mingguo HuangDepartment of Urology, and Department of Clinical Pathology, Akita 11 University Graduate School of Medicine, 1-1-1 Hondo, Akita, 010-8543, Japan. huangmg0319@yahoo.co.jp.
Shintaro NaritaDepartment of Urology, and Department of Clinical Pathology, Akita 11 University Graduate School of Medicine, 1-1-1 Hondo, Akita, 010-8543, Japan.
Hiromi SatoDepartment of Urology, and Department of Clinical Pathology, Akita 11 University Graduate School of Medicine, 1-1-1 Hondo, Akita, 010-8543, Japan.
Yuya SekineDepartment of Urology, and Department of Clinical Pathology, Akita 11 University Graduate School of Medicine, 1-1-1 Hondo, Akita, 010-8543, Japan.
Mizuki KobayashiDepartment of Urology, and Department of Clinical Pathology, Akita 11 University Graduate School of Medicine, 1-1-1 Hondo, Akita, 010-8543, Japan.
Soki KashimaDepartment of Urology, and Department of Clinical Pathology, Akita 11 University Graduate School of Medicine, 1-1-1 Hondo, Akita, 010-8543, Japan.
Ryohei YamamotoDepartment of Urology, and Department of Clinical Pathology, Akita 11 University Graduate School of Medicine, 1-1-1 Hondo, Akita, 010-8543, Japan.
Atsushi KoizumiDepartment of Urology, and Department of Clinical Pathology, Akita 11 University Graduate School of Medicine, 1-1-1 Hondo, Akita, 010-8543, Japan.
Taketoshi NaraDepartment of Urology, and Department of Clinical Pathology, Akita 11 University Graduate School of Medicine, 1-1-1 Hondo, Akita, 010-8543, Japan.
Kazuyuki NumakuraDepartment of Urology, and Department of Clinical Pathology, Akita 11 University Graduate School of Medicine, 1-1-1 Hondo, Akita, 010-8543, Japan.
Mitsuru SaitoDepartment of Urology, and Department of Clinical Pathology, Akita 11 University Graduate School of Medicine, 1-1-1 Hondo, Akita, 010-8543, Japan.
Hiroshi NanjoDepartment of Urology, and Department of Clinical Pathology, Akita 11 University Graduate School of Medicine, 1-1-1 Hondo, Akita, 010-8543, Japan.
Takayuki IkezoeDepartment of Hematology, Fukushima Medical University, Fukushima, Japan.
Tomonori HabuchiDepartment of Urology, and Department of Clinical Pathology, Akita 11 University Graduate School of Medicine, 1-1-1 Hondo, Akita, 010-8543, Japan.

Funding

Japan Society for the Promotion of Science 24K12479
6 · The paper itself

Abstract

backgroundInsulin-like growth factor (IGF) binding protein-2 (IGFBP2) is a secretory protein that modulate the activity of IGFs. It is highly expressed in various cancers such as prostate cancer (PCa), in which it may play a controversial role in tumor progression, however, the molecular mechanisms of IGFBP2 in PCa progression remain unclear.

methodsIn this study, we examined the expression pattern and role of IGFBP2 in PCa cells and the stroma during prostate tumor cell progression.

resultsIGFBP2 was highly expressed in LNCaP cells and prostate stromal fibroblasts (PrSC) and was mainly secreted by PrSCs. Tumor cell growth and invasiveness were not directly affected by treatment with IGFBP2 siRNAs (siIGFBP2) or recombinant IGFBP2 (rIGFBP2). However, decreased expression of IGFBP2 significantly increased PrSC activation and the secretion of pro-tumorigenic cytokines IL-6, IL-8, IP10, and CCL5 through upregulation of TGF-β, which subsequently enhanced prostate tumor cell progression. Clinically, low expression of stromal IGFBP2 was associated with a high reactive prostate stroma, advanced PCa progression, and increased IGFBP2 levels in the serum.

conclusionHere, we provide mechanistic evidence that IGFBP2 act as a critical regulatory factor in the activation of prostate stromal microenvironment and contributes to aggressive PCa progression.

Indexed as

Disease ProgressionInsulin-Like Growth Factor Binding Protein 2ProstateProstatic NeoplasmsStromal CellsCell Line, TumorCell ProliferationHumansMaleTransforming Growth Factor betaTumor MicroenvironmentIGFBP2 protein, humanInsulin-Like Growth Factor Binding Protein 2Transforming Growth Factor betaIGFBP2Insulin-like growth factor binding protein-2Prostate cancerProstate stromal cells

Identifiers

PMID41039587
PMCPMC12492507

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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.