{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMiR‐107 has emerged as a critical regulator in neurodegenerative disorders. In Alzheimer’s disease, its levels decline early and this deficit correlates with increased beta‐site amyloid precursor protein–cleaving enzyme 1 (BACE1) expression, along with associations to neuritic plaque and neurofibrillary tangle pathology."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "3"}]}, {"type": "t", "text": " In parallel, miR‐107 regulates granulin (GRN) expression—implicating it in frontotemporal dementia—and controls the translation of cytoskeletal components such as cofilin, thereby contributing to Alzheimer’s‐related neuritic rod formation."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "4"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn the realm of cancer biology, miR‐107 functions in a context‐dependent manner. In several gastric cancer models its dysregulation has been linked to the modulation of cell cycle regulators such as CDK6 and the transcription factor FOXO1, contributing either to growth inhibition or promotion of aggressive phenotypes, while its elevated expression in certain settings correlates with poor patient prognosis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "6", "end_ref": "10"}]}, {"type": "t", "text": " In colorectal cancer, miR‐107–mediated repression of metastasis suppressors like DAPK, KLF4 and modulation of the TINCR/miR‐107/CD36 axis has been implicated in enhanced invasiveness."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "11"}]}, {"type": "t", "text": " Moreover, studies in gastric and cervical cancers indicate additional targets—including FOXO1, NF1 and MCL1—through which miR‐107 influences proliferation, migration and invasion, while its altered circulating levels have also been proposed as biomarkers in breast cancer and its sequestration by long noncoding or circular RNAs (e.g. HULC, H19) further modulates oncogenic transcriptional programs."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "13", "end_ref": "21"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond neurodegeneration and oncogenesis, miR‐107 exerts diverse roles in metabolic and immune regulation. 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