Regional Activation of Myosin II in Cancer Cells Drives Tumor Progression via a Secretory Cross-Talk with the Immune Microenvironment

Mirella Georgouli(King's College London), Cecilia Herráiz(King's College London), Eva Crosas‐Molist(Queen Mary University of London), Bruce Fanshawe(St Thomas' Hospital), Óscar Maiques(Queen Mary University of London), Anna Perdrix(Queen Mary University of London), Pahini Pandya(King's College London), Irene Rodríguez‐Hernández(Queen Mary University of London), Kristina M. Ilieva(St Thomas' Hospital), Gaia Cantelli(King's College London), Panagiotis Karagiannis(St Thomas' Hospital), Silvia Mele(St Thomas' Hospital), Hoyin Lam(King's College London), Debra H. Josephs(Guy's Hospital), Xavier Matías‐Guiu(Universitat de Lleida), Rosa M. Marti(Universitat de Lleida), Frank O. Nestlé(St Thomas' Hospital), José L. Orgaz(Queen Mary University of London), Ilaria Malanchi(The Francis Crick Institute), Gilbert O. Fruhwirth(St Thomas' Hospital), Sophia N. Karagiannis(St Thomas' Hospital), Victoria Sanz‐Moreno(Queen Mary University of London)
Cell
January 31, 2019
Cited by 172Open Access
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Abstract

tumor-associated macrophages and vessels. Proteomic analysis shows that ROCK-Myosin II activity in amoeboid cancer cells controls an immunomodulatory secretome, enabling the recruitment of monocytes and their differentiation into tumor-promoting macrophages. Both amoeboid cancer cells and their associated macrophages support an abnormal vasculature, which ultimately facilitates tumor progression. Mechanistically, amoeboid cancer cells perpetuate their behavior via ROCK-Myosin II-driven IL-1α secretion and NF-κB activation. Using an array of tumor models, we show that high Myosin II activity in tumor cells reprograms the innate immune microenvironment to support tumor growth. We describe an unexpected role for Myosin II dynamics in cancer cells controlling myeloid function via secreted factors.


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