{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMIR23A is increasingly recognized as a key regulator in the tumor microenvironment, acting via both cell‐intrinsic and intercellular communication mechanisms. In hepatocellular carcinoma cells under endoplasmic reticulum stress, exosomal MIR23A‐3p is released to up‐regulate PD‐L1 in macrophages, thereby promoting tumor cell escape from immune surveillance."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": " In addition, tumor‐infiltrating cytotoxic T lymphocytes show elevated MIR23A levels that suppress the expression of BLIMP‐1, impairing T‐cell effector function."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "2"}]}, {"type": "t", "text": " MIR23A is also enriched in exosomes released by tumor cells that have undergone epithelial–mesenchymal transition, and its extracellular transfer further elicits angiogenic responses via targeting regulators such as SIRT1."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "3"}]}, {"type": "t", "text": " Moreover, in nasopharyngeal carcinoma, MIR23A overexpression is associated with enhanced microvessel density and metastatic progression."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "5"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nMIR23A also plays an important role in metabolic reprogramming and tumor progression. In several cancers, the MYC oncogene represses MIR23A and MIR23B, which in turn modulate glutamine catabolism—a critical source of energy fueling tumor growth."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "6"}]}, {"type": "t", "text": " In human leukemic cells, NF‐κB p65 inhibits MIR23A expression, thereby relieving its repressive effect on glutaminase and facilitating glutamine utilization."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "7"}]}, {"type": "t", "text": " Adipocyte‐derived exosomal MIR23A/B has been shown to promote hepatocellular carcinoma cell growth, migration, and chemoresistance through modulation of the VHL/hypoxia‐inducible factor axis."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "8"}]}, {"type": "t", "text": " Furthermore, circulating MIR23A is found at elevated levels in coronary artery disease, and its inclusion in diagnostic miRNA signatures underscores its value as a non‐invasive biomarker."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "9"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nA multitude of studies demonstrate that MIR23A is a versatile modulator of cell fate, affecting apoptosis, epithelial–mesenchymal transition (EMT), and responses to therapy. In lung cancer cells, MIR23A is induced by TGF‐β in a Smad‐dependent manner to suppress E‐cadherin and promote EMT as well as gefitinib resistance."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "11"}]}, {"type": "t", "text": " In ovarian granulosa cells, elevated MIR23A promotes apoptosis by down‐regulating anti‐apoptotic XIAP and engaging the FasL–Fas pathway."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "12"}]}, {"type": "t", "text": " Overexpression of the MIR23A~27A~24-2 cluster in HEK293T cells triggers both caspase‐dependent and ‐independent apoptosis, while in retinal pigment epithelial cells MIR23A modulates survival in response to oxidative stress."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "14"}]}, {"type": "t", "text": " In gastric and other cancers, MIR23A promotes proliferation and invasion by targeting key regulators such as IL6R, PDCD4, and by modulating autophagy through ATG12."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "16", "end_ref": "18"}]}, {"type": "t", "text": " In nasopharyngeal carcinoma, reduced MIR23A expression is linked to radioresistance via activation of the IL-8/Stat3 signaling pathway, and in hepatocellular carcinoma, MIR23A has been implicated in enhancing the antitumor efficacy of chemotherapeutics such as etoposide."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "19"}]}, {"type": "t", "text": " In lung cancer stem cells, elevated MIR23A contributes to resistance against EGFR‐targeted tyrosine kinase inhibitors by down‐regulating tumor suppressors including PTEN"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "21"}]}, {"type": "t", "text": ", and in glioma, MIR23A upregulation suppresses HOXD10 to facilitate invasion."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "22"}]}, {"type": "t", "text": " Additional studies document roles for MIR23A in modulating osteogenic differentiation, osteoarthritis pathogenesis, chemoresistance in colorectal cancer, and estrogen‐mediated apoptosis in liver cells via diverse targets such as SMAD3, ABCF1, and XIAP."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "23", "end_ref": "26"}]}, {"type": "t", "text": " MIR23A further contributes to melanoma and gastrointestinal cancer metastasis by targeting ADCY1 and by modulating AP-1/NFAT4-driven suppression of E-cadherin."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "27"}]}, {"type": "t", "text": " Its regulatory portfolio is expanded by its targeting of telomere-associated TRF2 to induce senescence"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "29"}]}, {"type": "t", "text": ", involvement in DNA damage repair via down-regulation of FANCG"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "30"}]}, {"type": "t", "text": ", and interference with osteogenic differentiation."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "31"}]}, {"type": "t", "text": " Moreover, MIR23A has been linked to the regulation of inflammatory signaling in rheumatoid arthritis by directly targeting IKKα"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "32"}]}, {"type": "t", "text": "and to autophagy regulation in the context of photoaging by modulating AMBRA1."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "33"}]}, {"type": "t", "text": " Finally, MIR23A’s oncogenic properties are further underscored in non‐small cell lung cancer stem cells and other contexts, emphasizing its dynamic influence on cell survival and therapeutic responses."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "21"}, {"type": "fg_f", "ref": "35"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its roles in cancer, comprehensive reviews and biomarker studies have highlighted the broader regulatory scope of MIR23A as part of the conserved MIR23A~27A~24-2 cluster."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "36"}]}, {"type": "t", "text": " Differential miRNA profiling in the circulation has identified MIR23A as a promising component of non‐invasive diagnostic panels."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "37"}]}, {"type": "t", "text": " In prostate cancer, decreased MIR23A levels correlate with increased metastatic potential and altered cytoskeletal dynamics"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "38"}]}, {"type": "t", "text": ", while bioactive compounds such as osthole modulate its expression to influence E-cadherin levels and cell motility."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "39"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Jiatao Liu, Lulu Fan, Hanqing Yu, et al. 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