作者: Natalia Filippova , Louis B. Nabors
关键词:
摘要: Homotypic and heterotypic cell fusions via permanent membrane temporal tunneling nanotube formations in the glioma microenvironment were recently documented vitro vivo mediate survival, plasticity, recurrence. Chronic inflammation, a hypoxic environment, aberrant mitochondrial function, ER stress due to unfolded protein accumulation upregulate fusion events, which leads tumor heterogeneity represents an adaptive mechanism promote survival plasticity cytotoxic, nutrient-deprived, mechanically stressed, inflammatory microenvironments. Cell is multistep process, consists of activation cellular response, autophagy formation, rearrangement cytoskeletal architecture areas cell-to-cell contacts, expression proinflammatory cytokines fusogenic proteins. The mRNA-binding ELAV-family HuR critical node, orchestrates architecture, overexpressed gliomas associated with poor prognosis treatment resistance. Our review provides link between role regulation potential suppression these processes by different classes inhibitors.