Evidence map›Paper›PMID 40878116›Full record

ArticleThe world journal of men's health2026

EGFL7 Inhibits the Immune Response in Metastatic Castration-Resistant Prostate Cancer by Deactivating Endothelial Intercellular Adhesion Molecule-1.

Seung Soo Lee, Ji Young Lee, Hyun Jung Lee, Sung-Woo Park

Abstract read
In one paragraph

Article in The world journal of men's health, 2026. 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

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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

4 authors.

Seung Soo LeeDepartment of Urology, Pusan National University School of Medicine, Yangsan, Korea.ORCID https://orcid.org/0000-0001-7856-6766
Ji Young LeeDepartment of Urology, Pusan National University School of Medicine, Yangsan, Korea.ORCID https://orcid.org/0000-0001-9690-1986
Hyun Jung LeeDepartment of Pathology, Pusan National University Yangsan Hospital, Pusan National University School of Medicine, Yangsan, Korea.ORCID https://orcid.org/0000-0002-2995-6060
Sung-Woo ParkDepartment of Urology, Pusan National University School of Medicine, Yangsan, Korea.ORCID https://orcid.org/0000-0002-9895-3461

Funding

National Research Foundation of Korea 2021R1A2C1009085
6 · The paper itself

Abstract

purposeEpidermal growth factor-like 7 (EGFL7) has been implicated in various cancers, but its role in different stages of prostate cancer (PCa), particularly metastatic castration-resistant prostate cancer (mCRPC), remains unclear. This study aimed to investigate the biological function of EGFL7 and its association with immune regulation in PCa. MATERIALS AND

methodsWe quantified EGFL7 and intercellular adhesion molecule-1 (ICAM-1) levels in serum and prostate tissue specimens from patients with benign prostatic hyperplasia (BPH), localized PCa, and mCRPC. To explore its functional role, EGFL7 expression was either silenced or overexpressed in DU145 and PC3 cells using siRNA or pCMV-GFP, respectively. Xenograft experiments were conducted in nude mice using transfected DU145/PC3 cells, followed by post-hoc microarray analysis of tumor tissues.

resultsOur findings revealed that EGFL7 expression was significantly higher in both serum and tumor tissues of mCRPC patients compared to those with BPH or localized PCa. ICAM-1 levels were inversely correlated with EGFL7 expression. Knockdown of EGFL7 in DU145 cells suppressed cell proliferation, migration, and invasion, while

conclusionsThese findings suggest that EGFL7 overexpression in mCRPC suppresses immune cell infiltration by downregulating endothelial ICAM-1. Our study highlights the potential of EGFL7 as a therapeutic target in advanced PCa.

Indexed as

Cell adhesion moleculesEndotheliumEpidermal growth factorImmune evasionProstatic neoplasms

Identifiers

PMID40878116
PMCPMC13302972

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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.