Cellular communication governs fundamental aspects of cell behavior. Remarkably, in the context of cancer, cells actively establish communication channels, fostering a cohesive matrix rather than existing as isolated entities. This study utilizes computational modeling to investigate the impact of diffusible secreted factors, operating through autocrine and paracrine signaling, on coordinating cancer cell motility and invasive mechanisms. Our approach focuses on self-generated gradients for chemotactic movement; however, signals from each cancer cell integrate locally, forming a unique signal field that guides cell movement. Our framework accounts for cell heterogeneity in signal emission properties, influencing communication intensity and range, as well as cellular response/preference. Cells may exhibit preferential responses to specific values within the signaling field, ranging from attraction to repulsion. In scenarios of synchronous signaling molecule secretion, a cell-density-dependent signal field emerges, influencing behavior based on local population density. Variations in cell response may, in that case, reflect differences in adhesive properties, outlining the continuum spectrum of endothelium-mesenchymal transition. Additionally, we explore the hypothesis that cell responses are not fixed but adaptively change as a nonlinear function of local cell density, implying phenotypic plasticity. Our agent-based model utilizes cellular automata on a 2D grid to depict individual cancer cells, allowing for proliferation, movement, and quiescence due to contact inhibition. Each cell emits a signal represented by a 2D Gaussian, with the signals collectively forming a signal field through Gaussian filtering. Diverse invasive patterns and expansion dynamics were observed. Cell communication not only facilitates invasion but also enables cells to self-organize based on their responses. In an initially heterogeneous population of signal emitters and non-emitters, a spatial hierarchy emerges, with emitters propelling the invasive front and developing morphological asymmetries and protrusions.. Introducing density-dependent phenotypic plasticity in cell response, cancer cell colonization was observed as an emergent property. A subset of cells invades distant regions, establishing new colonies iteratively. An in vitro exploration of these hypotheses is anticipated.