| Literature DB >> 29946782 |
Abstract
KEY POINTS: Cancer-associated fibroblasts (CAFs), a major component of the tumor microenvironment (TME), play an important role in cancer initiation, progression, and metastasis. Recent findings have demonstrated that the TME not only provides physical support for cancer cells, but also directs cell-to-cell interactions (in this case the interaction between cancer cells and CAFs). As cancer progresses, the CAFs also co evolve—transitioning from an inactivated state to an activated state. The elucidation and understanding of the interaction between cancer cells and CAFs will pave the way for new cancer therapies [1–3]. The TME is a heterogeneous environment consisting of fibroblasts, tumor-associated macrophages, adipocytes, an extracellular matrix, and mesenchymal stem cells [4]. The exact composition of each stroma varies depending on cancer and tissue type. To add to this variation, there is heterogeneity even within the CAF population itself. Different CAFs express different markers and influence stromal pro-tumorigenic capacity and cancer progression in diverse ways [5, 6].Entities:
Keywords: CAF-derived exosomes; Cancer-associated fibroblasts; Glutamine metabolism; Hypoxia-inducible factor-1; Reverse Warburg effect
Mesh:
Year: 2018 PMID: 29946782 DOI: 10.1007/978-3-319-77736-8_11
Source DB: PubMed Journal: Adv Exp Med Biol ISSN: 0065-2598 Impact factor: 2.622