{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nSNAI2, also known as Slug, is a zinc‐finger transcriptional repressor that plays a pivotal role in initiating the epithelial–mesenchymal transition (EMT) by directly binding to E‐box elements of epithelial adhesion gene promoters (for example, E‑cadherin) to silence their transcription. This loss of cell–cell adhesion is central to both embryonic morphogenesis and the progression of carcinomas, as SNAI2 induction—triggered by signals such as transforming growth factor β (TGF‑β), Notch activation, and other microenvironmental cues—facilitates the conversion to a mesenchymal, migratory phenotype. In diverse settings ranging from cardiac cushion morphogenesis to breast cancer recurrence, SNAI2 cooperates with other EMT regulators (including SNAI1, Twist1, and MRTFs) to promote apoptosis resistance and enhanced cell motility."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "11"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its function in driving EMT, SNAI2 is instrumental in promoting tumor invasiveness and metastatic progression through its capacity to enhance cancer stem cell‐like features and to regulate key signaling networks. Aberrant expression or dysregulation of SNAI2 has been associated with adverse clinical outcomes in a variety of cancers—including neural crest–derived disorders, esophageal squamous cell carcinoma, breast, melanoma, and colorectal tumors—by integrating signals from inflammatory cytokines, Notch, phosphatidylinositol 3‑kinase/AKT, and other oncogenic pathways. This integration results in increased expression of matrix metalloproteinases and altered adhesion molecule profiles that augment cell motility and enable invasive growth, thereby reprogramming the tumor microenvironment in favor of metastasis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "12", "end_ref": "31"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nSNAI2 activity is further fine‐tuned by complex regulatory networks that include noncoding RNAs and post‑translational modifications. MicroRNAs—such as miR‑203 and miR‑218—and long noncoding RNAs like SNHG15 can directly target or stabilize SNAI2, establishing feedback loops that regulate its expression. Moreover, additional regulatory layers mediated by hypoxic or metabolic stress conditions, via MEK/ERK and ATF4‐dependent pathways, as well as modulation by Notch signaling, contribute to the dynamic control of SNAI2. 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