Abstract
Tumor initiation, growth, invasion, and metastasis occur as a consequence of a complex interplay between the host environment and cancer cells. Fibroblasts are now recognized as a key host cell type involved in host–cancer signaling. This review discusses some recent studies that highlight the roles of fibroblasts in tumor initiation, early progression, invasion, and metastasis. Some clinical studies describing the prognostic significance of fibroblast-derived markers and signatures are also discussed.
Highlights
Tumor initiation, growth, invasion, and metastasis occur as a consequence of a complex interplay between the host environment and cancer cells
It is well recognized that tumor initiation, growth, invasion, and metastasis are a consequence of a complex interplay between the host environment and the cancer cell
Special attention is given to studies that indicate fibroblasts as critical components of tumor initiation, early progression, and various steps of the metastatic process (Figure 1)
Summary
Using different mouse models for inflammation-induced gastric cancer, the study of Quante et al showed that CAF precursors appeared in the bone-marrow already during chronic inflammation and increased during carcinogenesis These smooth muscle actin (ASMA)-positive cells, possibly derived from mesenchymal stem cells in a TGFb-dependent manner, were more potent than non-bone-marrow-derived fibroblasts in promotion of tumor growth and dissemination [26]. An interesting and somewhat surprising finding in this study was that PEG2 expression and the ability to induce CSCs were not strongly associated with the origin of the fibroblasts Taken together, these studies indicate CAFs as important components of a cancer stem cell niche providing regulating factors such as IL-6, BMP antagonists, and factors activating canonical and non-canonical Wnt signaling. Based on the strong evidence for a niche-dependent regulation of CSCs, it is justified to suggest targeting of these interactions as a strategy for therapeutic CSC depletion
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