Abstract
The role of inflammation in the development of cancer was described as early as the nineteenth century. Abundant evidence supports the preposition that various cancers are triggered by infection and chronic inflammatory disease whereas, evading immune destruction has been proposed as one of the new “hallmarks of cancer.” Changes of the tumor microenvironment have been closely correlated to cancer-mediated inflammation. Hyaluronan (HA), an important extracellular matrices component, has become recognized as an active participant in inflammatory, angiogenic, fibrotic, and cancer promoting processes. This review discusses how HA and specific HA-binding proteins participate in and regulate cancer-related inflammatory processes.
Highlights
The role of inflammation in the development of cancer was described as early as the nineteenth century
Extracellular matrices (ECMs) represent a complex network of proteins and glycosaminoglycans (GAGs), which define the structure of tissues in vivo and are critically important for cell growth, survival as well as differentiation, and key Abbreviations: DAMP, damage-associated molecular-pattern; ECMs, extracellular matrices; GAGs, glycosaminoglycans; HA, hyaluronan; HAS, hyaluronan synthases; HMWHA, high molecular weight HA; LMWHA, low molecular weight hyaluronan; HYAL, hyaluronidases; RHAMM, receptor for hyaluronan-mediated motility; ICAM-1, intercellular adhesion molecule 1; MAPKs, mitogen-activated protein kinases; MMP, matrix metalloprotease; TNF, tumor necrosis factor; TNF-alpha, tumor necrosis factor-alpha
Significant changes can be observed in the properties of ECM components, which deregulate the behavior of stromal cells, promote tumor-associated angiogenesis and inflammation, and lead to generation of a tumorigenic microenvironment [11–14]
Summary
The role of inflammation in the development of cancer was described as early as the nineteenth century. Significant changes can be observed in the properties of ECM components, which deregulate the behavior of stromal cells, promote tumor-associated angiogenesis and inflammation, and lead to generation of a tumorigenic microenvironment [11–14].
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