Microenvironment and tumor cell plasticity: an easy way out

Abstract

Cancer cells undergo genetic changes allowing their adaptation to environmental changes, thereby obtaining an advantage during the long metastatic route, disseminated of several changes in the surrounding environment. In particular, plasticity in cell motility, mainly due to epigenetic regulation of cancer cells by environmental insults, engage adaptive strategies aimed essentially to survive in hostile milieu, thereby escaping adverse sites. This review is focused on tumor microenvironment as a collection of structural and cellular elements promoting plasticity and adaptive programs. We analyze the role of extracellular matrix stiffness, hypoxia, nutrient deprivation, acidity, as well as different cell populations of tumor microenvironment.

Keywords: Acidity; CA; CAFs; Cell motility; Cell plasticity; ECM; EMT; EPC; Extracellular matrix; HGF; HIF-1; Hypoxia; Keap-1; LOX; MAT; MCT; MMP; Microenvironment; NF-E2-related factor; NF-κB; Nrf-2; OS; PCa; PK; PPP; ROS; SDF-1; TEM; TGF-β1; VEGF; cancer-associated fibroblasts; carbonic anhydrases; endothelial precursor cell; epithelial–mesenchymal transition; extracellular matrix; hepatocyte growth factor; hypoxia-inducible factor-1; kelch-like ECH-associated protein 1; lysyl oxidase; mesenchymal-amoeboid transition; metalloproteases; monocarboxylate transporter; nuclear factor-κB; oxidative stress; penthose phosphate pathway; prostate carcinoma; pyruvate kinase; reactive oxygen species; stromal cell-derived factor-1; trans-endothelial migration; tumor growth factor-β1; vascular endothelial growth factor.