Experiments have shown that mechanical stress can regulate many cellular processes. However, in most cases, the exact regulatory mechanisms are still not well understood. One approach in improving our understanding of such mechanically induced regulation is the quantitative study of cell deformation under an externally applied stress. In this paper, an axisymmetric finite-element model is developed and used to study the deformation of single, suspended fibroblasts in an optical stretcher in which a stretching force is applied onto the surface of the cell. A feature of our physical model is a viscoelastic material equation whose parameters vary spatially to mimic the experimentally observed spatial heterogeneity of cellular material properties. Our model suggests that cell size is a more important factor in determining the maximal strain of the optically stretched fibroblasts compared to the thickness of the actin cortical region. This result could explain the higher deformability observed experimentally for malignant fibroblasts in the optical stretcher. Our model also shows that maximal stress propagates into the nuclear region for malignant fibroblasts whereas for normal fibroblasts, it does not. We discuss how this may impact the transduction of cancer signaling pathways.