{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMicroRNA‐200b is a key member of the miR‐200 family that plays a central role in maintaining the epithelial phenotype and preventing epithelial–mesenchymal transition (EMT) across a number of biological and pathological settings. Several studies have demonstrated that miR‐200b exerts tumor‐suppressive functions by directly targeting mRNAs encoding transcriptional repressors of E‐cadherin such as ZEB1, ZEB2, SUZ12, SIP1 and ZFHX1B. As a result, miR‐200b restores E‐cadherin expression and suppresses the acquisition of mesenchymal traits, thereby inhibiting cancer stem cell formation and the invasive behavior seen in aggressive tumors."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "5"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn a variety of cancer models, miR‐200b has been shown to counteract EMT‐related changes and modulate tumor progression. In experimental systems including pancreatic and tongue squamous cell carcinomas, re‐expression of miR‐200b reduces chemoresistance and invasiveness through downregulation of key effectors—for example, by targeting SUZ12 in cancer stem cell formation or interfering with BMI1 expression in prostate cancer. In vascular and uterine models, the delivery of miR‐200b mimics suppresses angiogenic responses by directly targeting regulators such as Ets‐1, while in kidney and intestinal disease models its upregulation ameliorates fibrotic changes through restoration of epithelial markers."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "6", "end_ref": "17"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its classical role in regulating EMT, miR‐200b participates in diverse regulatory networks that impact cancer cell behavior and other disease processes. For instance, in breast, prostate and non‐small cell lung cancers, decreased miR‐200b levels correlate with enhanced metastatic properties and poor clinical outcome, with its restoration limiting cell proliferation, migration, and even vasculogenic mimicry by targeting molecules such as BMI1, PDGFR signaling components, Foxf2 and actin‐cytoskeleton effectors. Moreover, studies have revealed that RNA editing events altering miR‐200b’s sequence can shift its target repertoire—diminishing its capacity to repress ZEB1/2 while enabling suppression of new metastasis‐inhibitory targets like LIFR. In addition, miR‐200b influences innate immune signaling by repressing MyD88, and its levels in exosomes have been linked to disease aggressiveness in ovarian and colon cancers. Finally, its deregulation is observed in non‐cancer conditions such as Alzheimer’s disease and inflammatory bowel or Crohn’s disease, where miR‐200b impacts APP processing and fibrogenesis, respectively. 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