{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMiR‐106b—most commonly expressed as part of the miR‐106b–25 polycistronic cluster—has emerged as a critical oncogenic modulator in a variety of human malignancies. Its overexpression in cancers such as gastric, prostate, hepatocellular, and glioma has been shown to promote cell cycle progression through direct downregulation of tumor‐suppressors like CDKN1A (p21) and apoptotic mediators, while establishing negative feedback loops with transcription factors such as E2F1 and cooperating with its host gene MCM7 to fuel unchecked cellular proliferation and transformation. In addition, miR‐106b directly targets key regulators including caspase‐7, thereby modulating apoptotic pathways that further contribute to tumorigenesis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "17"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond driving proliferation, miR‐106b plays a pivotal role in tumor progression by promoting epithelial–mesenchymal transition (EMT), cellular migration, invasion, and therapeutic resistance. Its upregulation is associated with enhanced focal adhesion dynamics and cell motility, partly via suppression of pro‐apoptotic regulators (such as Bim and EP300) and modulation of key signaling cascades. Notably, miR‐106b can be transferred intercellularly via exosomes—such as those secreted by cancer‐associated fibroblasts—to confer chemoresistance (for instance, to agents like gemcitabine in pancreatic cancer), while altered circulating levels of this miRNA offer promise as noninvasive biomarkers for early detection and prognosis in malignancies including gastric and colorectal cancers."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "18", "end_ref": "38"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nMoreover, miR‐106b functions within complex regulatory networks that extend its influence beyond canonical oncogenic pathways. It is intricately involved in feedback loops with long noncoding RNAs and RNA‐binding proteins that modulate miRNA processing and transcription factor activity, thereby impacting diverse processes including neurodegeneration. 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