Cells produce mechanical forces for their physiological functions primarily via a non-equilibrium biopolymer network called the actin cytoskeleton. Myosin motors walk on actin filaments (F-actin) in the actin cytoskeleton, which results in the generation of tensile forces. Forces produced by the actomyosin contractility mediate various biomechanical phenomena in non-muscle cells at multiple length-scales. For example, it endows the actin cytoskeleton with non-equilibrium viscoelastic properties. It also drives morphological transformations of cells often accompanied by large-scale flow of the actin cytoskeleton during biological processes, such as cell migration, cytokinesis, and morphogenesis. In addition, contractile forces originating from the actomyosin contractility enable cells to structurally remodel surrounding extracellular matrices (ECMs) as well as to mechanically communicate with other cells for physiological and pathophysiological phenomena including wound healing, capillary morphogenesis, and cancer metastasis. Although the actomyosin contractility has been studied for decades due to its significance, it is still very challenging to illuminate how forces produced from the actomyosin contractility facilitate diverse phenomena at multiple length-scales by only experiments. Computational models are able to provide insights into understanding of intrinsic mechanisms by predicting and interpreting experimental results and by perturbing systems in ways that experiments cannot use. Since 2017, we have used computational models to address two fundamental questions regarding actomyosin contractility: how forces are produced from actomyosin contractility and how forces are translated to cellular and tissue levels and thus mediate matrix remodeling. For next two years, we will focus on addressing two new questions: i) how contractile forces govern cell shape changes and cell-scale cytoskeletal flow and ii) how cells embedded in ECM communicate with other cells via mechanical forces.