Deciphering the loop of epithelial-mesenchymal transition, inflammatory cytokines and cancer immunoediting. (August 2017)

• Record Type: Journal Article
• Authors: Sistigu, Antonella; Di Modugno, Francesca; Manic, Gwenola; Nisticò, Paola
• Is Part Of: Cytokine & growth factor reviews. Volume 36(2017)
• Page Start: 67
• Page End: 77
• Publication Date: 2017-08
• Subjects: AKT1/AKT AKT serine/threonine kinase 1 -- AXL AXL receptor tyrosine kinase -- Bmi1 BMI1 proto-oncogene, polycomb ring finger -- CAF cancer-associated fibroblast -- CDH/CAD cadherin -- CRKL CRK Like Proto-Oncogene -- CSC cancer stem cell -- CSF-1 colony-stimulating factor-1 -- CTLA4 cytotoxic T-lymphocyte antigen 4 -- CXCL C-X-C motif ligand -- CXCR C-X-C chemokine receptor -- ECM extracellular matrix -- EGF epidermal growth factor -- EMT epithelial–mesenchymal transition -- ESRP epithelial splicing regulatory protein -- FGF fibroblast growth factor -- FSP-1 fibroblast-specific protein-1 -- HDAC3 histone deacetylase 3 -- HGF hepatocyte growth factor -- HIF-1α hypoxia-inducible factor-1α -- ICB immune checkpoint blocker -- IFN-γ interferon-γ -- IL interleukin -- IL-6/8 R IL-6/8 receptor -- IRAK-M interleukin-1 receptor-associated kinase-M -- JAK Janus kinase -- KRAS Kirsten rat sarcoma viral oncogene homolog -- LOX lysyl oxidase -- LOXL2 lysyl oxidase like 2 -- MDSC myeloid-derived suppressor cell -- MET mesenchymal-epithelial transition -- MHC-I major histocompatibility complex-I -- miRNA microRNA -- MMP metalloproteinase -- NF-κB nuclear factor-κB -- NLRP3 NACHT, LRR and PYD domains-containing protein 3 -- NSCLC non-small cell lung cancer -- PDGF platelet-derived growth factor -- PD-L1 programmed death-ligand 1 -- Rac1 ras-related C3 botulinum toxin substrate 1 -- ROS reactive oxygen species -- α-SMA α-smooth muscle actin -- SMAD2 SMAD family member 2 -- SNAI1/SNAIL snail family transcriptional repressor 1 -- SNAI2/SLUG snail family transcriptional repressor 2 -- Sox9 SRY-box 9 -- STAT3 signal transducer and activator of transcription 3 -- TAM tumor-associated macrophage -- TAZ tafazzin -- TGF-β tumor growth factor-β -- TME tumor microenvironment -- TNF-α tumor necrosis factor-α -- TP53/p53 tumor suppressor p53 -- TWIST1/TWIST twist family bHLH transcription factor 1 -- VEGF vascular endothelial growth factor -- YAP1/YAP yes associated protein 1 -- ZEB1 zinc finger E-box-binding homeobox 1; EMT -- Tumor microenvironment -- Tumor immunoediting -- CSC; Cytokines -- Periodicals; 571.84
• DOI: 10.1016/j.cytogfr.2017.05.008
• Languages: English
• ISSNs: 1359-6101

Abstract

Graphical abstract: Highlights: Tumorigenesis and tumor progression depend on cell–cell interaction, cell-ECM interaction and soluble cues ( i.e. cytokines, growth factors). Innate and adaptive immunity shapes tumor fate and the phenotypic plasticity is a common feature of epithelial and immune cells. EMT is a physiological and coordinated program in which epithelial cells acquire motile phenotype and the characteristics of mesenchymal cells. In tumors EMT is a leading process regulating cancer invasion, cell phenotypic heterogeneity, stemness, immune escape and resistance to therapy. EMT is induced by the cooperation of signaling pathways activated by the dialogue between tumor cells and stromal cells in an inflammatory TME. Abstract: Tumorigenesis and tumor progression relies on the dialectics between tumor cells, the extracellular matrix and its remodelling enzymes, neighbouring cells and soluble cues. The host immune response is crucial in eliminating or promoting tumor growth and the reciprocal coevolution of tumor and immune cells, during disease progression and in response to therapy, shapes tumor fate by activating innate and adaptive mechanisms. The phenotypic plasticity is a common feature of epithelial and immune cells and epithelial-mesenchymal transition (EMT) is a dynamic process, governed by microenvironmental stimuli, critical in tumor cell shaping, increased tumor cell heterogeneity and stemness. In this review we will outline how the dysregulation of microenvironmental signaling is crucial in determining tumor plasticity and EMT, arguing how therapy resistance hinges on these dynamics.