CAF-derived exosomes drive the FGF4/SHH feedback loop by encapsulating GREM1 in non-small cell lung cancer

Abstract Background One of the hallmarks of a pre-metastatic niche (PMN) is the infiltration of immunosuppressive macrophages, while the mechanism remains largely uncharted. Here, we reveal that cancer-associated fibroblasts-derived exosomes (CAF-exo) polarize macrophages towards an immunosuppressiv...

Full description

Saved in:
Bibliographic Details
Main Authors: Xianqiao Wu, Wei Chen, Tianzheng Fang, Ziyuan Chen, Shuai Fang, Chengwei Zhou
Format: Article
Language:English
Published: BMC 2025-08-01
Series:Molecular Medicine
Subjects:
Online Access:https://doi.org/10.1186/s10020-025-01340-0
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1849226209581334528
author Xianqiao Wu
Wei Chen
Tianzheng Fang
Ziyuan Chen
Shuai Fang
Chengwei Zhou
author_facet Xianqiao Wu
Wei Chen
Tianzheng Fang
Ziyuan Chen
Shuai Fang
Chengwei Zhou
author_sort Xianqiao Wu
collection DOAJ
description Abstract Background One of the hallmarks of a pre-metastatic niche (PMN) is the infiltration of immunosuppressive macrophages, while the mechanism remains largely uncharted. Here, we reveal that cancer-associated fibroblasts-derived exosomes (CAF-exo) polarize macrophages towards an immunosuppressive phenotype through encapsulating Gremlin-1 (GREM1) in non-small cell lung cancer (NSCLC). Methods CAF and normal fibroblasts (NF) were extracted from NSCLC patients, and the exosomes produced were extracted. The effects of NF- or CAF-derived exosomes on the expression of PMN-associated markers and macrophage M2 polarization markers in mouse lung and liver tissues were compared. CAF-exo-mediated macrophage phenotypic switching and immunosuppressive effects on T cells were studied in vitro. Orthotopic lung tumors were formed in mice using Lewis lung carcinoma (LLC) cells, followed by CAF-exo treatment. CAF-exo with GREM1 knockdown were used to treat macrophages or the LLC model mice. Finally, the reciprocal regulation between GREM1 and FGF4/SHH in macrophages was revealed, and rescue experiments were conducted. Results Intravenous injection of CAF-exo induced an immunosuppressive phenotype of macrophages in lung and liver tissues, leading to PMN formation. Tumor progression promoted by CAF-exo was blocked by knocking down GREM1 in CAF-exo. CAF-exo-derived GREM1 activated FGF4/SHH signaling in macrophages, and knockdown of FGF4/SHH inhibited macrophage M2 polarization. Ectopic expression of SHH or FGF4 activated GREM1/FGF4/SHH signaling and rescued the anti-tumor effects of GREM1 knockdown in vivo. Conclusions CAF-exo activated the positive feedback regulation of FGF4/SHH and GREM1 in macrophages by carrying GREM1, leading to the switch of macrophages to an immunosuppressive phenotype and PMN formation in NSCLC.
format Article
id doaj-art-5d0a7a2cef7c4d268a4d51b465d56a96
institution Kabale University
issn 1528-3658
language English
publishDate 2025-08-01
publisher BMC
record_format Article
series Molecular Medicine
spelling doaj-art-5d0a7a2cef7c4d268a4d51b465d56a962025-08-24T11:35:08ZengBMCMolecular Medicine1528-36582025-08-0131111910.1186/s10020-025-01340-0CAF-derived exosomes drive the FGF4/SHH feedback loop by encapsulating GREM1 in non-small cell lung cancerXianqiao Wu0Wei Chen1Tianzheng Fang2Ziyuan Chen3Shuai Fang4Chengwei Zhou5Department of Thoracic Surgery, The First Affiliated Hospital of Ningbo UniversityHealth Science Center, Ningbo UniversityHealth Science Center, Ningbo UniversityHealth Science Center, Ningbo UniversityDepartment of Thoracic Surgery, The First Affiliated Hospital of Ningbo UniversityDepartment of Thoracic Surgery, The First Affiliated Hospital of Ningbo UniversityAbstract Background One of the hallmarks of a pre-metastatic niche (PMN) is the infiltration of immunosuppressive macrophages, while the mechanism remains largely uncharted. Here, we reveal that cancer-associated fibroblasts-derived exosomes (CAF-exo) polarize macrophages towards an immunosuppressive phenotype through encapsulating Gremlin-1 (GREM1) in non-small cell lung cancer (NSCLC). Methods CAF and normal fibroblasts (NF) were extracted from NSCLC patients, and the exosomes produced were extracted. The effects of NF- or CAF-derived exosomes on the expression of PMN-associated markers and macrophage M2 polarization markers in mouse lung and liver tissues were compared. CAF-exo-mediated macrophage phenotypic switching and immunosuppressive effects on T cells were studied in vitro. Orthotopic lung tumors were formed in mice using Lewis lung carcinoma (LLC) cells, followed by CAF-exo treatment. CAF-exo with GREM1 knockdown were used to treat macrophages or the LLC model mice. Finally, the reciprocal regulation between GREM1 and FGF4/SHH in macrophages was revealed, and rescue experiments were conducted. Results Intravenous injection of CAF-exo induced an immunosuppressive phenotype of macrophages in lung and liver tissues, leading to PMN formation. Tumor progression promoted by CAF-exo was blocked by knocking down GREM1 in CAF-exo. CAF-exo-derived GREM1 activated FGF4/SHH signaling in macrophages, and knockdown of FGF4/SHH inhibited macrophage M2 polarization. Ectopic expression of SHH or FGF4 activated GREM1/FGF4/SHH signaling and rescued the anti-tumor effects of GREM1 knockdown in vivo. Conclusions CAF-exo activated the positive feedback regulation of FGF4/SHH and GREM1 in macrophages by carrying GREM1, leading to the switch of macrophages to an immunosuppressive phenotype and PMN formation in NSCLC.https://doi.org/10.1186/s10020-025-01340-0Non-small cell lung cancerPre-metastatic nicheCancer-associated fibroblastMacrophage polarizationGREM1
spellingShingle Xianqiao Wu
Wei Chen
Tianzheng Fang
Ziyuan Chen
Shuai Fang
Chengwei Zhou
CAF-derived exosomes drive the FGF4/SHH feedback loop by encapsulating GREM1 in non-small cell lung cancer
Molecular Medicine
Non-small cell lung cancer
Pre-metastatic niche
Cancer-associated fibroblast
Macrophage polarization
GREM1
title CAF-derived exosomes drive the FGF4/SHH feedback loop by encapsulating GREM1 in non-small cell lung cancer
title_full CAF-derived exosomes drive the FGF4/SHH feedback loop by encapsulating GREM1 in non-small cell lung cancer
title_fullStr CAF-derived exosomes drive the FGF4/SHH feedback loop by encapsulating GREM1 in non-small cell lung cancer
title_full_unstemmed CAF-derived exosomes drive the FGF4/SHH feedback loop by encapsulating GREM1 in non-small cell lung cancer
title_short CAF-derived exosomes drive the FGF4/SHH feedback loop by encapsulating GREM1 in non-small cell lung cancer
title_sort caf derived exosomes drive the fgf4 shh feedback loop by encapsulating grem1 in non small cell lung cancer
topic Non-small cell lung cancer
Pre-metastatic niche
Cancer-associated fibroblast
Macrophage polarization
GREM1
url https://doi.org/10.1186/s10020-025-01340-0
work_keys_str_mv AT xianqiaowu cafderivedexosomesdrivethefgf4shhfeedbackloopbyencapsulatinggrem1innonsmallcelllungcancer
AT weichen cafderivedexosomesdrivethefgf4shhfeedbackloopbyencapsulatinggrem1innonsmallcelllungcancer
AT tianzhengfang cafderivedexosomesdrivethefgf4shhfeedbackloopbyencapsulatinggrem1innonsmallcelllungcancer
AT ziyuanchen cafderivedexosomesdrivethefgf4shhfeedbackloopbyencapsulatinggrem1innonsmallcelllungcancer
AT shuaifang cafderivedexosomesdrivethefgf4shhfeedbackloopbyencapsulatinggrem1innonsmallcelllungcancer
AT chengweizhou cafderivedexosomesdrivethefgf4shhfeedbackloopbyencapsulatinggrem1innonsmallcelllungcancer