The role of tumor microenvironment in cancer progression is gaining significant attention. It is realized that cancer cells and the corresponding stroma co-evolve with time. Cancer cells recruit and transform the stromal cells, which in turn remodel the extra cellular matrix of the stroma. This complex interaction between the stroma and the cancer cells results in a dynamic feed-forward/feed-back loop with biochemical and biophysical cues that assist metastatic transition of the cancer cells. Although biochemistry has long been studied for the understanding of cancer progression, biophysical signaling is emerging as a critical paradigm determining cancer metastasis. In this mini review, we discuss the role of one of the biophysical cues, mostly the mechanical stiffness of tumor microenvironment, in cancer progression and its clinical implications.
Keywords: ADAMs, Adamalysins; ANGPT2, Angiopoietin 2; Activin/TGFβ; CAF, Cancer associated fibroblast; CSF-1, Colony stimulating factor 1; CTGF, Connective tissue growth factor; CYR61/CCN1, Cysteine-rich angiogenic inducer 61/CCN family member 1; Cancer; ECM stiffness; ECM, Extracellular matrix; EGF, Epidermal growth factor; EMT, Epithelial to mesenchymal transition; FGF, Fibroblast growth factor; Growth factors; HGF/SF, Hepatocyte growth factor/Scatter factor; IGFs, Insulin-like growth factors; IL-13, Interleukin-13; IL-33, Interleukin-33; IL-6, Interleukin-6; KGF, Keratinocyte growth factor, also FGF7; LOX, Lysyl Oxidase; MMPs, Matrix metalloproteinases; Metastasis; NO, Nitric oxide; SDF-1/CXCL12, Stromal cell-derived factor 1/C-X-C motif chemokine 12; TACs, Tumor-associated collagen signatures; TGFβ, Transforming growth factor β; TNF-α, Tumor necrosis factor-α; Tumor biophysics; VEGF, Vascular endothelial growth factor; α-SMA, α-Smooth muscle actin.