The extra-cellular matrix (ECM) is a source of biochemical and biomechanical influences that direct cell proliferation and fate. The molecular mechanisms underlying the interplay between these influences and tissue homeostasis nevertheless remain relatively ill-defined. The ROCK signalling pathway lies at the interface between mechanical and biochemical signalling. We have previously demonstrated 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 the mechanisms by which cancers in which ROCK is hyperactivated recruit and educate fibroblasts. ROCK-educated fibroblasts are more effective at producing and remodelling the ECM and cause accelerated tumour progression. Furthermore, mimicking the cancer micro-environment of enhanced compressive stress rapidly activates the Rho-ROCK pathway in cancer cells and in tissues. As this pathway in turn regulates the key 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 fibroblast phenotypes and thereby the ECM may be a novel therapeutic approach to target cancers.