Exosomal circPACRGL promotes progression of colorectal cancer via the miR-142-3p/miR-506-3p- TGF-β1 axis.


Journal

Molecular cancer
ISSN: 1476-4598
Titre abrégé: Mol Cancer
Pays: England
ID NLM: 101147698

Informations de publication

Date de publication:
27 07 2020
Historique:
received: 09 02 2020
accepted: 21 07 2020
entrez: 28 7 2020
pubmed: 28 7 2020
medline: 29 5 2021
Statut: epublish

Résumé

Colorectal cancer (CRC) is the leading cause of cancer-related death worldwide. Exosome shave emerged as crucial regulators of intercellular communication and that abundant Circular RNAs (circRNAs) are enriched within exosomes. CircRNAs are novel members of noncoding RNAs regulating cancer proliferation and progression. However, the function and regulatory mechanism of cancer-derived exosomal circRNAs in CRC remains unclear. CRC cells-derived exosomes were characterized using transmission electron microscopy, nanoparticle tracking analysis (NTA) and western blot. CCK-8, wound healing and transwell assays, and flow cytometry assays were conducted to assess whether exosomes would affect the proliferation, metastasis, and apoptosis of CRC cells, respectively. Moreover, we performed the RNA sequencing and RT-qPCR to identify circRNAs in exosome-stimulated CRC cells. Fluorescence in situ hybridization (FISH) assay was used to detect the cellular distribution of circPACRGL. Bioinformatic analyses (StarBase 2.0) were used to pool the miRNA targets of circPACRGL. Luciferase assays were performed to verify the direct interaction. Finally, flow cytometry was used to detect the differentiation of N1-N2 neutrophils. Our study identified a novel CRC-derived exosomal circRNA, circPACRGL. We found circPACRGL was significantly upregulated in CRC cells after tumor-derived exosomes addition. Moreover, circPACRGL serves as a sponge for miR-142-3p/miR-506-3p to facilitate the transforming growth factor-β1 (TGF-β1) expression. As a result, circPACRGL promoted CRC cell proliferation, migration and invasion, as well as differentiation of N1 to N2 neutrophils via miR-142-3p/miR-506-3p-TGF-β1 axis. Our study, the first to reveal that cancer-derived exosomal circPACRGL plays an oncogenic role in CRC proliferation and metastasis, providing mechanistic insights into the roles of circRNAs in CRC progression and a valuable marker for CRC treatment.

Sections du résumé

BACKGROUND
Colorectal cancer (CRC) is the leading cause of cancer-related death worldwide. Exosome shave emerged as crucial regulators of intercellular communication and that abundant Circular RNAs (circRNAs) are enriched within exosomes. CircRNAs are novel members of noncoding RNAs regulating cancer proliferation and progression. However, the function and regulatory mechanism of cancer-derived exosomal circRNAs in CRC remains unclear.
METHODS
CRC cells-derived exosomes were characterized using transmission electron microscopy, nanoparticle tracking analysis (NTA) and western blot. CCK-8, wound healing and transwell assays, and flow cytometry assays were conducted to assess whether exosomes would affect the proliferation, metastasis, and apoptosis of CRC cells, respectively. Moreover, we performed the RNA sequencing and RT-qPCR to identify circRNAs in exosome-stimulated CRC cells. Fluorescence in situ hybridization (FISH) assay was used to detect the cellular distribution of circPACRGL. Bioinformatic analyses (StarBase 2.0) were used to pool the miRNA targets of circPACRGL. Luciferase assays were performed to verify the direct interaction. Finally, flow cytometry was used to detect the differentiation of N1-N2 neutrophils.
RESULTS
Our study identified a novel CRC-derived exosomal circRNA, circPACRGL. We found circPACRGL was significantly upregulated in CRC cells after tumor-derived exosomes addition. Moreover, circPACRGL serves as a sponge for miR-142-3p/miR-506-3p to facilitate the transforming growth factor-β1 (TGF-β1) expression. As a result, circPACRGL promoted CRC cell proliferation, migration and invasion, as well as differentiation of N1 to N2 neutrophils via miR-142-3p/miR-506-3p-TGF-β1 axis.
CONCLUSION
Our study, the first to reveal that cancer-derived exosomal circPACRGL plays an oncogenic role in CRC proliferation and metastasis, providing mechanistic insights into the roles of circRNAs in CRC progression and a valuable marker for CRC treatment.

Identifiants

pubmed: 32713345
doi: 10.1186/s12943-020-01235-0
pii: 10.1186/s12943-020-01235-0
pmc: PMC7384220
doi:

Substances chimiques

MIRN142 microRNA, human 0
MIRN506 microRNA, human 0
MicroRNAs 0
RNA, Circular 0
TGFB1 protein, human 0
Transforming Growth Factor beta1 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

117

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Auteurs

Anquan Shang (A)

Department of Laboratory Medicine, Shanghai Tongji Hospital, Tongji University School of Medicine, No. 389, Xincun Road, Putuo District, Shanghai, 200065, P.R. China.

Chenzheng Gu (C)

Department of Laboratory Medicine, Shanghai Tongji Hospital, Tongji University School of Medicine, No. 389, Xincun Road, Putuo District, Shanghai, 200065, P.R. China.

Weiwei Wang (W)

Department of Pathology, The Sixth People's Hospital of Yancheng City, Yancheng, 224001, P.R. China.

Xuan Wang (X)

Department of Pharmacy, Putuo People's Hospital, Tongji University School of Medicine, Shanghai, 200060, P.R. China.

Junjun Sun (J)

Department of Laboratory Medicine, Shanghai Tongji Hospital, Tongji University School of Medicine, No. 389, Xincun Road, Putuo District, Shanghai, 200065, P.R. China.

Bingjie Zeng (B)

Department of Laboratory Medicine, Shanghai Tongji Hospital, Tongji University School of Medicine, No. 389, Xincun Road, Putuo District, Shanghai, 200065, P.R. China.

Chen Chen (C)

Department of Laboratory Medicine, Shanghai Tongji Hospital, Tongji University School of Medicine, No. 389, Xincun Road, Putuo District, Shanghai, 200065, P.R. China.

Wenjing Chang (W)

Department of Laboratory Medicine, Shanghai Tongji Hospital, Tongji University School of Medicine, No. 389, Xincun Road, Putuo District, Shanghai, 200065, P.R. China.

Yili Ping (Y)

Department of Laboratory Medicine, Shanghai Tongji Hospital, Tongji University School of Medicine, No. 389, Xincun Road, Putuo District, Shanghai, 200065, P.R. China.

Ping Ji (P)

Department of Laboratory Medicine, Shanghai Tongji Hospital, Tongji University School of Medicine, No. 389, Xincun Road, Putuo District, Shanghai, 200065, P.R. China.

Junlu Wu (J)

Department of Laboratory Medicine, Shanghai Tongji Hospital, Tongji University School of Medicine, No. 389, Xincun Road, Putuo District, Shanghai, 200065, P.R. China.

Wenqiang Quan (W)

Department of Laboratory Medicine, Shanghai Tongji Hospital, Tongji University School of Medicine, No. 389, Xincun Road, Putuo District, Shanghai, 200065, P.R. China.

Yiwen Yao (Y)

Department of Internal Medicine V-Pulmonology, Allergology, Respiratory Intensive Care Medicine, Saarland University Hospital, 66424, Homburg, Germany.

Yongxin Zhou (Y)

Department of Thoracic-cardiovascular Surgery, Shanghai Tongji Hospital,Tongji University School of Medicine, No. 389, Xincun Road, Putuo District, Shanghai, 200065, P.R. China. zhou6302@tongji.edu.cn.

Zujun Sun (Z)

Department of Laboratory Medicine, Shanghai Tongji Hospital, Tongji University School of Medicine, No. 389, Xincun Road, Putuo District, Shanghai, 200065, P.R. China. sunzujun@tongji.edu.cn.

Dong Li (D)

Department of Laboratory Medicine, Shanghai Tongji Hospital, Tongji University School of Medicine, No. 389, Xincun Road, Putuo District, Shanghai, 200065, P.R. China. lidong@tongji.edu.cn.

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Classifications MeSH