Cancer-associated fibroblasts induce metalloprotease-independent cancer cell invasion of the basement membrane

Alexandros Glentis, Philipp Oertle, Pascale Mariani, Aleksandra Chikina, Fatima El Marjou, Youmna Attieh, Francois Zaccarini, Marick Lae, Damarys Loew, Florent Dingli, Philemon Sirven, Marie Schoumacher, Basile G. Gurchenkov, Marija Plodinec and Danijela Matic Vignjevic ()
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Alexandros Glentis: PSL Research University
Philipp Oertle: University of Basel
Pascale Mariani: Curie Institute
Aleksandra Chikina: PSL Research University
Fatima El Marjou: PSL Research University
Youmna Attieh: PSL Research University
Francois Zaccarini: PSL Research University
Marick Lae: Curie Institute
Damarys Loew: PSL Research University, Laboratoire de spectrométrie de masse protéomique
Florent Dingli: PSL Research University, Laboratoire de spectrométrie de masse protéomique
Philemon Sirven: Institut Curie, PSL Research University
Marie Schoumacher: PSL Research University
Basile G. Gurchenkov: PSL Research University
Marija Plodinec: University of Basel
Danijela Matic Vignjevic: PSL Research University

Nature Communications, 2017, vol. 8, issue 1, 1-13

Abstract: Abstract At the stage of carcinoma in situ, the basement membrane (BM) segregates tumor cells from the stroma. This barrier must be breached to allow dissemination of the tumor cells to adjacent tissues. Cancer cells can perforate the BM using proteolysis; however, whether stromal cells play a role in this process remains unknown. Here we show that an abundant stromal cell population, cancer-associated fibroblasts (CAFs), promote cancer cell invasion through the BM. CAFs facilitate the breaching of the BM in a matrix metalloproteinase-independent manner. Instead, CAFs pull, stretch, and soften the BM leading to the formation of gaps through which cancer cells can migrate. By exerting contractile forces, CAFs alter the organization and the physical properties of the BM, making it permissive for cancer cell invasion. Blocking the ability of stromal cells to exert mechanical forces on the BM could therefore represent a new therapeutic strategy against aggressive tumors.

Date: 2017
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DOI: 10.1038/s41467-017-00985-8

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