{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nZEB1 is a pivotal transcription factor that orchestrates epithelial‐to‐mesenchymal transition (EMT) by directly repressing key epithelial markers such as E‐cadherin and critical cell–cell adhesion and polarity genes. Its up‐regulation in a variety of cancers—including breast, colorectal, pancreatic, and lung carcinomas—is strongly associated with dedifferentiation, increased motility, invasiveness, and ultimately metastatic dissemination, thereby contributing to poor clinical outcomes. This early role of ZEB1 in driving the mesenchymal phenotype is underscored by its direct transcriptional repression of epithelial determinants and its correlation with tumor progression."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "15"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nZEB1 is intricately regulated by microRNAs—most notably the miR-200 family and miR-205—that form reciprocal feedback loops with it to fine-tune the balance between epithelial and mesenchymal states. Attenuation or loss of these microRNAs leads to sustained high levels of ZEB1, which not only reinforces EMT but also promotes tumor-initiating properties, stemness, drug resistance, and radioresistance across multiple cancer types. In addition, ZEB1 modulates key signaling pathways such as those mediated by transforming growth factor-β (TGF-β) and p53, integrating diverse upstream signals to further drive malignant progression."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "16", "end_ref": "31"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its cell‐intrinsic effects, ZEB1 critically shapes the tumor microenvironment. It orchestrates interactions that lead to remodeling of the extracellular matrix—such as enhanced collagen deposition and crosslinking via lysyl oxidase family members—and activates downstream kinases (e.g., FAK/SRC) that further potentiate invasion and metastatic spread. 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