Evidence map›Paper›PMID 40234961›Full record

ArticleBiology direct2025

Colon cancer exosome-associated HSP90B1 initiates pre-metastatic niche formation in the liver by polarizing M1 macrophage into M2 phenotype.

ShuJie Li, Xue Fu, Deng Ning, QiuMeng Liu, JunFang Zhao, Qi Cheng, XiaoPing Chen, Li Jiang

Abstract read
In one paragraph

Article in Biology direct, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing 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

15 citing papers in PubMed.

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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

8 authors.

ShuJie LiDepartment of Biliary-Pancreatic Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science & Technology, Wuhan, 430022, China.
Xue FuDepartment of Biliary-Pancreatic Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science & Technology, Wuhan, 430022, China.
Deng NingDepartment of Hepatobiliary Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
QiuMeng LiuHubei Key Laboratory of Hepato-Pancreato-Biliary Diseases, Wuhan, 430030, Hubei, China.
JunFang ZhaoDepartment of Biliary-Pancreatic Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science & Technology, Wuhan, 430022, China.
Qi ChengHubei Key Laboratory of Hepato-Pancreato-Biliary Diseases, Wuhan, 430030, Hubei, China.
XiaoPing ChenHubei Key Laboratory of Hepato-Pancreato-Biliary Diseases, Wuhan, 430030, Hubei, China.
Li JiangDepartment of Biliary-Pancreatic Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science & Technology, Wuhan, 430022, China. prof_jiang2023@163.com.

Funding

National Natural Science Foundation of China 81472705Natural Science Foundation of Hubei Province 2021CFB391
6 · The paper itself

Abstract

backgroundColorectal cancer (CRC) frequently metastasizes to the liver, worsening patient outcomes. The formation of a pre-metastatic niche (PMN) is essential for this process, but how the primary colon tumor orchestrates the PMN formation remains unclear.

methodsThis study investigated the role of CRC-derived exosomes using CT-26 murine colon carcinoma cells. The effects of these exosomes on immune cells, specifically M1 macrophage polarization and CD8 + T cell viability, were assessed. HSP90B1 expression in CT-26-derived exosomes was analyzed to understand its contribution to PMN formation. HSP90B1 silencing experiments were conducted to evaluate its impact on immunosuppressive PMN creation and liver metastasis. Patient blood samples were also examined to correlate exosomal HSP90B1 levels with CRC progression.

resultsExosomes from CT-26 cells were found to polarize M1 macrophages into an M2 phenotype and decrease CD8 + T cell viability, promoting liver metastasis. High expression of HSP90B1 in CT-26 cell-derived exosomes was identified as a key factor in inducing M2 macrophage polarization and creating an immunosuppressive PMN. Silencing HSP90B1 significantly inhibited the exosome-mediated formation of the immunosuppressive PMN and reduced liver metastasis. Furthermore, elevated levels of HSP90B1 in patient-derived exosomes were associated with advanced CRC and poorer prognosis.

conclusionsCRC-derived exosomes promote liver metastasis by forming an immunosuppressive PMN through HSP90B1. Targeting HSP90B1 in CRC exosomes may offer a new therapeutic strategy to prevent liver metastasis and improve patient outcomes.

Indexed as

Colonic NeoplasmsExosomesHSP90 Heat-Shock ProteinsLiver NeoplasmsMacrophagesAnimalsCD8-Positive T-LymphocytesCell Line, TumorHumansMicePhenotypeTumor MicroenvironmentHSP90 Heat-Shock ProteinsColon cancerExosomeHSP90B1Macrophage polarizationPre-metastatic Nich

Identifiers

PMID40234961
PMCPMC12001560

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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.