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Título: | Diverse matrix metalloproteinase functions regulate cancer amoeboid migration |
Autor: | Orgaz, José L. CSIC ORCID; Pandya, Pahini; Dalmeida, Rimple; Karagiannis, Panagiotis; Sánchez-Laorden, Berta CSIC ORCID; Viros, Amaya; Albrengues, Jean; Nestle, Frank O.; Ridley, Anne J.; Gaggioli, Cedric; Marais, Richard; Karagiannis, Sophia N.; Sanz-Moreno, Victoria | Fecha de publicación: | 2014 | Editor: | Springer Nature | Citación: | Nature Communications 5: 4255 (2014) | Resumen: | Rounded-amoeboid cancer cells use actomyosin contractility driven by Rho-ROCK and JAK-STAT3 to migrate efficiently. It has been suggested that rounded-amoeboid cancer cells do not require matrix metalloproteinases (MMPs) to invade. Here we compare MMP levels in rounded-amoeboid and elongated-mesenchymal melanoma cells. Surprisingly, we find that rounded-amoeboid melanoma cells secrete higher levels of several MMPs, including collagenase MMP-13 and gelatinase MMP-9. As a result, rounded-amoeboid melanoma cells degrade collagen I more efficiently than elongated-mesenchymal cells. Furthermore, using a non-catalytic mechanism, MMP-9 promotes rounded-amoeboid 3D migration through regulation of actomyosin contractility via CD44 receptor. MMP-9 is upregulated in a panel of rounded-amoeboid compared with elongated-mesenchymal melanoma cell lines and its levels are controlled by ROCK-JAK-STAT3 signalling. MMP-9 expression increases during melanoma progression and it is particularly prominent in the invasive fronts of lesions, correlating with cell roundness. Therefore, rounded-amoeboid cells use both catalytic and non-catalytic activities of MMPs for invasion. | Versión del editor: | https://doi.org/10.1038/ncomms5255 | URI: | http://hdl.handle.net/10261/307510 | DOI: | 10.1038/ncomms5255 | E-ISSN: | 2041-1723 |
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