The extra-cellular matrix (ECM) is a source of biochemical and biomechanical signals that regulate tissue homeostasis. However, the molecular mechanisms underlying the interplay between mechanical tension and tissue homeostasis are still relatively ill-defined. We have previously shown that ROCK signalling promotes epidermal proliferation and cutaneous tumour progression by increasing ECM production, elevating ECM stiffness and enhancing integrin-mediated mechanotransduction signalling in tumours. We now have new insight into a mechanism by which cancers direct the production of a tumour-promoting ECM. Hyperactivation of ROCK in a murine model of mammary cancer increases the secretion by tumour cells, of factors that cause the recruitment and education of stromal fibroblasts. These educated fibroblasts exhibit features and functions of cancer-associated fibroblasts and are associated with increased ECM production and enhanced tumour progression. Furthermore, we have shown that mimicking the early mammary cancer environment of enhanced compressive stress rapidly activates the Rho-ROCK pathway in cancer cells and in epithelial tissues. As this pathway in turn regulates the key tumour-promoting mechanical properties of the microenvironment, we propose that ROCK promotes cancer progression via a mechanoreciprocal feed-forward mechanism and that inhibiting the effectors of ROCK that regulate the ECM may be a novel therapeutic approach to target cancers via normalisation of the ECM.