Cytoneme-mediated signaling essential for tumorigenesis
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Abstract
Communication between neoplastic cells and cells of their microenvironment is critical to cancer progression. To investigate the role of cytoneme-mediated signaling as a mechanism for distributing growth factor signaling proteins between tumor and tumor-associated cells, we analyzed EGFR and RET Drosophila tumor models and tested several genetic loss-of-function conditions that impair cytoneme-mediated signaling. Neuroglian, capricious, Irk2, SCAR, and diaphanous are genes that cytonemes require during normal development. Neuroglian and Capricious are cell adhesion proteins, Irk2 is a potassium channel, and SCAR and Diaphanous are actin-binding proteins, and the only process to which they are known to contribute jointly is cytoneme-mediated signaling. We observed that diminished function of any one of these genes suppressed tumor growth and increased organism survival. We also noted that EGFR-expressing tumor discs have abnormally extensive tracheation (respiratory tubes) and ectopically express Branchless (Bnl, a FGF) and FGFR. Bnl is a known inducer of tracheation that signals by a cytoneme-mediated process in other contexts, and we determined that exogenous over-expression of dominant negative FGFR suppressed tumor growth. Our results are consistent with the idea that cytonemes move signaling proteins between tumor and stromal cells and that cytoneme-mediated signaling is required for tumor growth and malignancy.
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TGF-β induces TGFB1 expression.
“Since TGF-β induces TGFB1 expression246”
From TGFβ biology in cancer progression and immunotherapy (2021) · cites this paper as [246]
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- [22]González-Méndez L, Seijo-Barandiarán I, Guerrero I. Cytoneme-mediated cell-cell contacts for Hedgehog reception. Elife. 2017; 6 10.7554/eLife.24045 28825565 PMC5565369 · DOI
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- Authors
- Fereres, S., Hatori, R., Hatori, M., & Kornberg, T. B.
- Affiliations
- University of California, San Francisco (US)
- Corresponding author
- Kornberg, Thomas B.
- Venue
- PLOS Genetics
- Publisher
- Public Library of Science (PLoS)
- Published
- 2019-09-30
- Volume
- 15
- Issue
- 9
- Pages
- e1008415
- ISSN
- 1553-7390 (ISSN-L)
- 1553-7404
- PMC
- PMC6786653
- OpenAlex
- W2977454722
- Cited by
- 54
- References
- 50
- Citations by year
- 2026: 7 · 2025: 6 · 2024: 5 · 2023: 3 · 2022: 7 · 2021: 12 · 2020: 9 · 2019: 4 · 2018: 1
- FWCI
- 2.65
- Type
- journal article
- Language
- en
- Update notices
- new_version (2019-10-10)
- Open access
- gold
- doi.org
- Licence
- Locations
- PLoS Genetics (publishedVersion, cc-by)
- bioRxiv (Cold Spring Harbor Laboratory) (acceptedVersion)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- eScholarship (California Digital Library) (submittedVersion)
- eScholarship (California Digital Library) (submittedVersion, cc-by)
- Figshare (submittedVersion, cc-by)
- Funders
- National Cancer Institute (CA205580)
- National Institutes of Health (T32HL007731, 2T32HL007185)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Axon Guidance and Neuronal Signaling
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular Mechanics and Interactions
- Keywords
- tumor microenvironment, EGFR, RET, Neuroglian, scar tissue, Diaphanous, actin cytoskeleton, FGF signaling, fibroblast growth factor receptor, tumor stromal cells, tumor growth, cell adhesion, potassium channels
- MeSH terms
- Animals, Cell Transformation, Neoplastic, Drosophila melanogaster, Neoplasm Metastasis, Neoplasms, Pseudopodia, Wings, Animal, Signal Transduction, Receptors, Invertebrate Peptide, Cell Membrane Structures, Models, Animal, Drosophila Proteins, Intercellular Signaling Peptides and Proteins, Tumor Microenvironment, Imaginal Discs, Carcinogenesis, ErbB Receptors
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