The impact of cancer-associated fibroblast-derived exosomes on the malignant transformation of the breast cancer microenvironment

Tumor microenvironment (TME) promotes breast cancer progression through complex cellular interactions. Extracellular vesicles derived from cancer-associated fibroblasts (CAF-EXO) are increasingly being studied as important mediators in this process. Still, their specific roles in the epithelial-mesenchymal transition (EMT) of breast cancer cells have not been fully elucidated. The purpose of this study was to evaluate the potential effects of CAF-EXO on the proliferation, apoptosis, migration, invasion, and EMT of breast cancer cells. MDA-MB-231 cells were treated with normal fibroblast-derived exosomes (HKF-EXO) or CAF-derived exosomes (CAF-EXO), and the effects of the exosomes on cell proliferation (CCK-8), apoptosis (Annexin V/7-AAD), migration/invasion (Transwell), and the expressions of EMT markers (RT-PCR, Western blot) were evaluated. The results showed that compared with the control group, CAF-EXO significantly enhanced the proliferation, migration, and invasion abilities of the cells, while reducing cell apoptosis. The expression of E-cadherin was reduced in MDA-MB-231 cells treated with CAF-EXO, while the expression of N-cadherin and LC3B was increased. These results suggested that exosomes derived from CAF may promote the malignant progression of breast cancer by inducing proliferation, invasion, and EMT of breast cancer cells, thereby providing preliminary evidence for understanding their role in TME remodeling.

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Publication Details

Journal
CYTOLOGIA
Published
2026-06-24
DOI
https://doi.org/10.1508/cytologia.91.111
Primary Topic
Extracellular vesicles in disease
Type
article
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article

The impact of cancer-associated fibroblast-derived exosomes on the malignant transformation of the breast cancer microenvironment

J J, Puerkaiti Paierhati, Muzhapaer Abudukeremu, Fangfang Li et al.
CYTOLOGIA
Extracellular vesicles in disease
article

The impact of cancer-associated fibroblast-derived exosomes on the malignant transformation of the breast cancer microenvironment

J J, Puerkaiti Paierhati, Muzhapaer Abudukeremu, Fangfang Li, Shuangshuang Li, Binlin Ma
article en

Abstract

Tumor microenvironment (TME) promotes breast cancer progression through complex cellular interactions. Extracellular vesicles derived from cancer-associated fibroblasts (CAF-EXO) are increasingly being studied as important mediators in this process. Still, their specific roles in the epithelial-mesenchymal transition (EMT) of breast cancer cells have not been fully elucidated. The purpose of this study was to evaluate the potential effects of CAF-EXO on the proliferation, apoptosis, migration, invasion, and EMT of breast cancer cells. MDA-MB-231 cells were treated with normal fibroblast-derived exosomes (HKF-EXO) or CAF-derived exosomes (CAF-EXO), and the effects of the exosomes on cell proliferation (CCK-8), apoptosis (Annexin V/7-AAD), migration/invasion (Transwell), and the expressions of EMT markers (RT-PCR, Western blot) were evaluated. The results showed that compared with the control group, CAF-EXO significantly enhanced the proliferation, migration, and invasion abilities of the cells, while reducing cell apoptosis. The expression of E-cadherin was reduced in MDA-MB-231 cells treated with CAF-EXO, while the expression of N-cadherin and LC3B was increased. These results suggested that exosomes derived from CAF may promote the malignant progression of breast cancer by inducing proliferation, invasion, and EMT of breast cancer cells, thereby providing preliminary evidence for understanding their role in TME remodeling.

CYTOLOGIAVol. 91(2)
Xinjiang Medical University (CN), Tumor Hospital of Xinjiang Medical University (CN), Heze Municipal Hospital (CN)
Good health and well-being
Openalex Percentile: Top 11%
Extracellular vesicles in disease
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The impact of cancer-associated fibroblast-derived exosomes on the malignant transformation of the breast cancer microenvironment — J J, Puerkaiti Paierhati, et al. · CYTOLOGIA (2026) | TGRS Research Map | TGRS