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外泌体非编码RNA在癌症相关成纤维细胞介导的治疗耐药中的作用(综述)

Role of exosomal non‑coding RNAs in cancer‑associated fibroblast‑mediated therapy resistance (Review).

作者信息

Li Junxin, Huang Yu, Fu Lin, Shi Ming, Hu Gongli, Du Fei, Wang Zhongshu, Xiao Yi, Zhang Yan, Li Yanyu

机构信息

Department of Pharmacy, Zigong Fourth People's Hospital, Zigong, Sichuan 643000, P.R. China.

Department of Pharmacy, The Fourth Affiliated Hospital of Southwest Medical University, Meishan, Sichuan 620000, P.R. China.

出版信息

Int J Oncol. 2025 Aug;67(2). doi: 10.3892/ijo.2025.5774. Epub 2025 Jul 19.


DOI:10.3892/ijo.2025.5774
PMID:40682844
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12274182/
Abstract

Cancer‑associated fibroblasts (CAFs) represent an important component of the stromal cell population within the tumor microenvironment (TME) and are intricately linked to tumor growth, metastasis and drug resistance. In the TME, non‑coding RNAs present in exosomes act as essential mediators of intercellular communication. Exosomal RNAs derived from cancer cells activate CAFs, which in turn regulate cancer cell proliferation, invasion and drug resistance. Conversely, exosomal RNAs derived from CAFs contribute to therapeutic resistance in cancer by modulating survival signaling pathways, epithelial‑mesenchymal transition, programmed cell death, drug transporter expression levels and immune evasion. The present review examines the role and mechanisms of exosomal RNAs in CAF‑mediated cancer therapeutic resistance and offers recommendations for future research based on the underlying mechanisms of CAF‑induced drug resistance.

摘要

癌症相关成纤维细胞(CAFs)是肿瘤微环境(TME)中基质细胞群体的重要组成部分,与肿瘤生长、转移和耐药性密切相关。在TME中,外泌体中存在的非编码RNA是细胞间通讯的重要介质。源自癌细胞的外泌体RNA激活CAFs,进而调节癌细胞的增殖、侵袭和耐药性。相反,源自CAFs的外泌体RNA通过调节生存信号通路、上皮-间质转化、程序性细胞死亡、药物转运蛋白表达水平和免疫逃避,促进癌症的治疗抵抗。本综述探讨了外泌体RNA在CAF介导的癌症治疗抵抗中的作用和机制,并根据CAF诱导耐药的潜在机制为未来研究提供建议。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/758d/12274182/e92a62741b72/ijo-67-02-05774-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/758d/12274182/d93e1883fbff/ijo-67-02-05774-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/758d/12274182/d4d83f131050/ijo-67-02-05774-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/758d/12274182/a4fb75210fe6/ijo-67-02-05774-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/758d/12274182/2ec1d1afbc95/ijo-67-02-05774-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/758d/12274182/e92a62741b72/ijo-67-02-05774-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/758d/12274182/d93e1883fbff/ijo-67-02-05774-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/758d/12274182/d4d83f131050/ijo-67-02-05774-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/758d/12274182/a4fb75210fe6/ijo-67-02-05774-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/758d/12274182/2ec1d1afbc95/ijo-67-02-05774-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/758d/12274182/e92a62741b72/ijo-67-02-05774-g04.jpg

相似文献

[1]
Role of exosomal non‑coding RNAs in cancer‑associated fibroblast‑mediated therapy resistance (Review).

Int J Oncol. 2025-8

[2]
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Med Oncol. 2025-7-1

[3]
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[4]
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[5]
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Adv Sci (Weinh). 2025-7

[6]
Unveiling the power of exosomal non-coding RNAs: key drivers of lung cancer progression in the tumor microenvironment.

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[7]
CAF-derived exosomal miR-196b-5p after androgen deprivation therapy promotes epithelial-mesenchymal transition in prostate cancer cells through HOXC8/NF-κB signaling pathway.

Biol Direct. 2025-7-4

[8]
Rab27aCAF exosomal miR-9-5p promotes osteosarcoma progression via CREBRF/MAPK signaling pathway.

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[9]
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[10]
The emerging roles of exosomes in tumor-stroma interaction.

J Cancer Res Clin Oncol. 2016-9

本文引用的文献

[1]
CAF-derived exosomal LINC01711 promotes breast cancer progression by activating the miR-4510/NELFE axis and enhancing glycolysis.

FASEB J. 2025-4-15

[2]
Role of Cancer Associated Fibroblast (CAF) derived miRNAs on head and neck malignancies microenvironment: a systematic review.

BMC Cancer. 2025-4-1

[3]
Endothelial-like cancer-associated fibroblasts facilitate pancreatic cancer metastasis via vasculogenic mimicry and paracrine signalling.

Gut. 2025-3-23

[4]
Targeting ncRNAs to overcome metabolic reprogramming‑mediated drug resistance in cancer (Review).

Int J Oncol. 2025-5

[5]
Cancer-associated fibroblasts promote EGFR-TKI resistance via the CTHRC1/glycolysis/H3K18la positive feedback loop.

Oncogene. 2025-5

[6]
Glycolysis reprogramming in CAFs promotes oxaliplatin resistance in pancreatic cancer through circABCC4 mediated PKM2 nuclear translocation.

Cell Death Dis. 2025-2-23

[7]
The role of exosomal non-coding RNAs in the breast cancer tumor microenvironment.

Funct Integr Genomics. 2025-2-1

[8]
Cancer drug resistance as learning of signaling networks.

Biomed Pharmacother. 2025-2

[9]
Apoptosis in Cancer Biology and Therapy.

Annu Rev Pathol. 2025-1

[10]
BATF2 inhibits the stem cell-like properties and chemoresistance of gastric cancer cells through PTEN/AKT/β-catenin pathway.

Theranostics. 2024-10-21

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