MicroRNAs transfer from human macrophages to hepato-carcinoma cells and inhibit proliferation
Open accessAbstract
Recent research has indicated a new mode of intercellular communication facilitated by the movement of RNA between cells. There is evidence that RNA can transfer between cells in a multitude of ways, including in complex with proteins or lipids or in vesicles, including apoptotic bodies and exosomes. However, there remains little understanding of the function of nucleic acid transfer between human cells. In this article, we report that human macrophages transfer microRNAs (miRNAs) to hepato-carcinoma cells (HCCs) in a manner that required intercellular contact and involved gap junctions. Two specific miRNAs transferred efficiently between these cells--miR-142 and miR-223--and both were endogenously expressed in macrophages and not in HCCs. Transfer of these miRNAs influenced posttranscriptional regulation of proteins in HCCs, including decreased expression of reporter proteins and endogenously expressed stathmin-1 and insulin-like growth factor-1 receptor. Importantly, transfer of miRNAs from macrophages functionally inhibited proliferation of these cancerous cells. Thus, these data led us to propose that intercellular transfer of miRNA from immune cells could serve as a new defense against unwanted cell proliferation or tumor growth.
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miRNAs transfer between co-cultured cells via direct cell-cell contact and gap junctions.
“miRNAs have also been shown to transfer between co-cultured cells via direct cell-cell contact and gap junctions (144).”
From Overview of MicroRNA Biogenesis, Mechanisms of Actions, and Circulation (2018) · cites this paper as [144]
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- Authors
- Aucher, A., Rudnicka, D., & Davis, D. M.
- Affiliations
- Imperial College London (GB)
- University of Manchester (GB)
- Corresponding author
- Aucher, Anne
- Rudnicka, Dominika
- ORCID
- Davis, Daniel M
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2013-12
- Volume
- 191
- Issue
- 12
- Pages
- 6250-6260
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- PMC
- PMC3858238
- OpenAlex
- W2095813909
- Cited by
- 247
- References
- 62
- Citations by year
- 2026: 5 · 2025: 10 · 2024: 20 · 2023: 18 · 2022: 26 · 2021: 21 · 2020: 30 · 2019: 24 · 2018: 16 · 2017: 21 · 2016: 19 · 2015: 19 · 2014: 18
- FWCI
- 6.56
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Immunology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Research Explorer (The University of Manchester) (submittedVersion)
- Funders
- Lister Institute of Preventive Medicine
- National University of Singapore
- Hebrew University of Jerusalem
- Chinese University of Hong Kong
- Medical Research Council
- Biotechnology and Biological Sciences Research Council (BB/I013407/2)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Extracellular vesicles in disease
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer-related molecular mechanisms research
- Keywords
- microRNA transfer, intercellular RNA transfer, macrophages, hepatocellular carcinoma, gap junctions, miR-142, miR-223, STMN1, IGF-1 receptor, post-transcriptional regulation, tumor cell proliferation, tumor microenvironment, immune cells
- MeSH terms
- Cell Communication, Cell Division, Cell Line, Transformed, Cytoskeleton, Carcinoma, Hepatocellular, Humans, Leukemia, Monocytic, Acute, Liver Neoplasms, Macrophages, Recombinant Fusion Proteins, Transfection, Gene Expression Regulation, Neoplastic, Receptor, IGF Type 1, Genes, Reporter, Coculture Techniques, Bridged Bicyclo Compounds, Heterocyclic, RNA, Small Interfering, Mastocytoma, MicroRNAs, Cell Line, Tumor, Stathmin, Thiazolidines, Cell-Derived Microparticles, Exosomes, Hep G2 Cells
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