{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nmiR‐206 has emerged as a multifunctional regulator with prominent tumor‐suppressive roles in diverse cancers. In breast and endometrial carcinomas, miR‐206 downregulates estrogen receptor‑α expression and its coregulators, while in gastric cancer it targets cyclin D2 to arrest cell cycle progression. In sarcomas such as rhabdomyosarcoma, it suppresses oncogenic drivers like c‑Met to inhibit cell proliferation and migration. Similarly, in lung cancers, miR‐206 downregulates c‑Met and Bcl2, thereby blocking epithelial–mesenchymal transition (EMT) and reducing invasiveness. Its activity has also been linked to breast cancer metabolic reprogramming via regulation of glycolytic enzymes and, in osteosarcoma, low miR‑206 expression correlates with poor prognosis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "14"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to these antitumor effects, miR‐206 plays critical roles in metabolic reprogramming and differentiation. Under conditions of sustained NRF2 signaling, miR‑206 levels are attenuated, which facilitates the redirection of glucose flux toward the pentose phosphate pathway; conversely, restoring miR‑206 expression rebalances metabolic gene expression. In the central nervous system, miR‑206 regulates brain‐derived neurotrophic factor (BDNF), thereby influencing memory function in Alzheimer’s disease. Its high, muscle‐specific expression is essential during myogenic differentiation, and in neuromuscular disorders such as amyotrophic lateral sclerosis, elevated circulating miR‑206 may serve as a compensatory response and a potential biomarker."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "15", "end_ref": "19"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its intrinsic effects on tumor cell behavior, miR‑206 modulates the tumor microenvironment and chemotherapeutic responses. By targeting Notch3, miR‑206 contributes to pro‐apoptotic signaling and modulates histone acetylation in certain hematologic malignancies. In lung cancer cells, overexpression of miR‑206 attenuates HGF‑induced EMT and angiogenesis via suppression of the c‑Met/PI3K/AKT/mTOR cascade. Notably, therapeutic delivery of miR‑206 through exosomes derived from bone marrow mesenchymal stem cells can be transferred to osteosarcoma cells to downregulate oncogenic factors (such as TRA2B), while sequestration of miR‑206 by long noncoding RNAs may underlie chemoresistance in breast cancer."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "20", "end_ref": "23"}, {"type": "fg_f", "ref": "12"}, {"type": "fg_f", "ref": "24"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nCirculating levels of miR‑206 also show promise as non‐invasive biomarkers for disease diagnosis and prognosis. Altered serum miR‑206 has been reported in rhabdomyosarcoma, osteosarcoma, and even in mild cognitive impairment, indicating its potential utility in monitoring disease progression and therapeutic outcomes. Together, these findings position miR‑206 as a multifaceted molecular regulator that interconnects oncogenic signaling, metabolic reprogramming, differentiation, and intercellular communication, thereby offering novel avenues for targeted therapies and biomarker development."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "26"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Elizabeth O'Day, Ashish Lal "}, {"type": "b", "children": [{"type": "t", "text": "MicroRNAs and their target gene networks in breast cancer."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Breast Cancer Res (2010)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1186/bcr2484"}], "href": "https://doi.org/10.1186/bcr2484"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "20346098"}], "href": "https://pubmed.ncbi.nlm.nih.gov/20346098"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Naoto Kondo, Tatsuya Toyama, Hiroshi Sugiura, et al. 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