Dynamic cell shape changes play an essential role in many processes, including directional migration and cancer invasion. In these processes, protrusive and contractile forces that are generated by cells, have to be controlled in space and time. Previous work has shown that small GTPases of the Rho family are master regulators of cell protrusion and contraction and that they play a central role in the spatio-temporal coordination of dynamic cell shape changes. In particular, an activator-inhibitor signal network that is based on the Rho family member RhoA can generate local, dynamic cell contraction pulses. The frequency and amplitude of these contraction pulses is dependent on the cytosolic concentration of a particular family of RhoA activators, the Lbc-type GEFs. These molecules participate in a positive feedback loop that can amplify RhoA activity to initiate a cell contraction pulse. Interestingly, upregulation of these contraction-inducing Lbc-type GEFs is often found in cancer and correlates with advanced stage tumors and invasive behavior. However, how these RhoGEFs contribute to tumor progression and which role cell contraction pulses play in these processes is still unclear. Here, we utilize an optogenetic approach to acutely control the cytosolic levels of the Lbc family member GEF-H1 in living cells. The system is based on a well-established tumor model, the B16F1 mouse melanoma cell line that can form multicellular tumor spheroids. Stable cell lines were generated that co-express the optogenetic system together with fluorescently tagged read-out proteins. This enabled direct investigation of the cellular response to light-controlled cell contraction dynamics via TIRF and spinning disk microscopy. As expected, an optogenetically-controlled increase of the cytosolic GEF-H1 levels induced increased cell contraction dynamics in individual, adherent cells. This increase in contraction dynamics was dependent on continuously elevated GEF-H1 levels and recovered quickly to baseline levels without further optogenetic perturbation. The optogenetically-induced increase in GEF-H1-mediated cell contraction dynamics resulted in enhanced cellular morphodynamics both in individual, adherent cells, and in spheroids cultured in a 3D collagen matrix. Interestingly, on the multi-cellular level, the enhanced dynamics of individual cells lead to an expansion of spheroids. Pharmacological manipulations revealed that this expansion was dependent on a central regulator of cell-matrix interactions, the focal adhesion kinase (FAK). This suggests that interactions between cells and the extracellular matrix (ECM) and signaling via cell-ECM contacts, plays a role in linking individual cell contraction dynamics to multi-cellular tumor behavior. Furthermore, long-term induction of GEF-H1-mediated contraction dynamics stimulated the escape of individual cells from the spheroid structure. Overall, these findings revealed a direct link between elevated levels of the Lbc family member GEF-H1, which stimulates cell contraction signal network dynamics, leading to an expansion of multicellular melanoma tumor spheroids and an increased invasive capacity indicated by the escape of individual cells into the surrounding matrix. We propose a mechanism, in which enhanced cell contractility contributes to tumor progression by stimulating the dynamics of cell-matrix contacts and by weakening cell-cell contacts, resulting in an asymmetric force at the border of the tumor, that pulls cells towards the surrounding matrix.