The DOI matches its Crossref record; 36 of the 36 references it cites were found in a registry or an index.
MET is required for the recruitment of anti-tumoural neutrophils
Open accessAbstract
Mutations or amplification of the MET proto-oncogene are involved in the pathogenesis of several tumours, which rely on the constitutive engagement of this pathway for their growth and survival. However, MET is expressed not only by cancer cells but also by tumour-associated stromal cells, although its precise role in this compartment is not well characterized. Here we show that MET is required for neutrophil chemoattraction and cytotoxicity in response to its ligand hepatocyte growth factor (HGF). Met deletion in mouse neutrophils enhances tumour growth and metastasis. This phenotype correlates with reduced neutrophil infiltration to both the primary tumour and metastatic sites. Similarly, Met is necessary for neutrophil transudation during colitis, skin rash or peritonitis. Mechanistically, Met is induced by tumour-derived tumour necrosis factor (TNF)-α or other inflammatory stimuli in both mouse and human neutrophils. This induction is instrumental for neutrophil transmigration across an activated endothelium and for inducible nitric oxide synthase production upon HGF stimulation. Consequently, HGF/MET-dependent nitric oxide release by neutrophils promotes cancer cell killing, which abates tumour growth and metastasis. After systemic administration of a MET kinase inhibitor, we prove that the therapeutic benefit of MET targeting in cancer cells is partly countered by the pro-tumoural effect arising from MET blockade in neutrophils. Our work identifies an unprecedented role of MET in neutrophils, suggests a potential ‘Achilles’ heel’ of MET-targeted therapies in cancer, and supports the rationale for evaluating anti-MET drugs in certain inflammatory diseases.
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Cites
HIF-1α is essential for myeloid cell-mediated inflammation
Cramer, T., Yamanishi, Y., Clausen, B. E., Förster, I., Pawlinski, R., Mackman, N., Haase, V. H., Jaenisch, R., Corr, M., Nizet, V., et al. (2003) · Cell · doi:10.1016/s0092-8674(03)00154-5 · Cited by 2,046
Targeting MET in cancer: rationale and progress
Gherardi, E., Birchmeier, W., Birchmeier, C., & Woude, G. V. (2012) · Nature Reviews Cancer · doi:10.1038/nrc3205 · Cited by 1,423
Bussolino, F., Di Renzo, M. F., Ziche, M., Bocchietto, E., Olivero, M., Naldini, L., Gaudino, G., Tamagnone, L., Coffer, A., & Comoglio, P. M. (1992) · The Journal of cell biology · doi:10.1083/jcb.119.3.629 · Cited by 1,337
Hypoxia promotes invasive growth by transcriptional activation of the met protooncogene
Pennacchietti, S., Michieli, P., Galluzzo, M., Mazzone, M., Giordano, S., & Comoglio, P. M. (2003) · Cancer Cell · doi:10.1016/s1535-6108(03)00085-0 · Cited by 1,311
Self-citationDrug development of MET inhibitors: targeting oncogene addiction and expedience
Comoglio, P. M., Giordano, S., & Trusolino, L. (2008) · Nature Reviews Drug Discovery · doi:10.1038/nrd2530 · Cited by 818
Haslett, C., Guthrie, L. A., Kopaniak, M. M., Johnston, R. B., & Henson, P. M. (1985) · PubMed Central · Cited by 779
Neutrophil function in inflammation and inflammatory diseases
Wright, H. L., Moots, R. J., Bucknall, R. C., & Edwards, S. W. (2010) · Rheumatology · doi:10.1093/rheumatology/keq045 · Cited by 761
Tumor-associated neutrophils: friend or foe?
Fridlender, Z. G., & Albelda, S. M. (2012) · Carcinogenesis · doi:10.1093/carcin/bgs123 · Cited by 699
Neufert, C., Becker, C., & Neurath, M. F. (2007) · Nature Protocols · doi:10.1038/nprot.2007.279 · Cited by 675
Choueiri, T. K., Vaishampayan, U., Rosenberg, J. E., Logan, T. F., Harzstark, A. L., Bukowski, R. M., Rini, B. I., Srinivas, S., Stein, M. N., Adams, L. M., et al. (2013) · Journal of Clinical Oncology · doi:10.1200/jco.2012.43.3383 · Cited by 463
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Understanding the tumor immune microenvironment (TIME) for effective therapy
Binnewies, M., Roberts, E. W., Kersten, K., Chan, V., Fearon, D. F., Merad, M., Coussens, L. M., Gabrilovich, D. I., Ostrand-Rosenberg, S., Hedrick, C. C., et al. (2018) · Nature Medicine · doi:10.1038/s41591-018-0014-x · Cited by 6,145
The evolving tumor microenvironment: From cancer initiation to metastatic outgrowth
de Visser, K. E., & Joyce, J. A. (2023) · Cancer Cell · doi:10.1016/j.ccell.2023.02.016 · Cited by 4,059
Roles of the immune system in cancer: From tumor initiation to metastatic progression
Gonzalez, H., Hagerling, C., & Werb, Z. (2018) · Genes & Development · doi:10.1101/gad.314617.118 · Cited by 2,111
Neutrophils in cancer: Neutral no more
Coffelt, S. B., Wellenstein, M. D., & de Visser, K. E. (2016) · Nature reviews. Cancer · doi:10.1038/nrc.2016.52 · Cited by 1,830
Neutrophil diversity and plasticity in tumour progression and therapy
Jaillon, S., Ponzetta, A., Di Mitri, D., Santoni, A., Bonecchi, R., & Mantovani, A. (2020) · Nature Reviews Cancer · doi:10.1038/s41568-020-0281-y · Cited by 1,285
Metadata
- Authors
- Finisguerra, V., Di Conza, G., Di Matteo, M., Serneels, J., Costa, S., Thompson, A. A. R., Wauters, E., Walmsley, S., Prenen, H., Granot, Z., Casazza, A., & Mazzone, M.
- Venue
- Nature
- Published
- 2015-05-18
- Volume
- 522
- Issue
- 7556
- Pages
- 349-353
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- OpenAlex
- W1920052832
- Cited by
- 492
- References
- 36
- FWCI
- 14.43
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Finisguerra, V., Di Conza, G., Di Matteo, M., Serneels, J., Costa, S., Thompson, A. A. R., Wauters, E., Walmsley, S., Prenen, H., Granot, Z., Casazza, A., & Mazzone, M. (2015). MET is required for the recruitment of anti-tumoural neutrophils. Nature. https://doi.org/10.1038/nature14407
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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