{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMIRLET7C is a multifunctional microRNA with prominent tumor‐suppressive roles. In various cancers—including non–small cell lung cancer, prostate cancer, hepatocellular carcinoma, cholangiocarcinoma, gastric and colorectal cancers—MIRLET7C is frequently down‐regulated, leading to the de‐repression of key oncogenic targets such as integrin β3, MAP4K3, the androgen receptor, and members of the Bcl family. This loss of regulation contributes to enhanced cell proliferation, resistance to apoptosis, increased metastatic propensity, and chemoresistance. In several studies, sponging of MIRLET7C by long non–coding RNAs (for example, H19, CCAT1, and SNHG6) further alleviates its suppressive effects on oncogenic pathways (e.g., PI3K/AKT/mTOR, Ras/NF‐κB), thereby promoting malignant progression and the acquisition of cancer stem cell–like properties."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "22"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nMIRLET7C also plays an essential role in the regulation of inflammatory and immune responses as well as in antiviral defense. In viral infections, for instance during influenza and dengue virus challenges, MIRLET7C is up‐regulated to directly target viral transcripts and mitigate replication. Its altered expression is associated with diverse immune‐mediated diseases such as major depression, where dysregulation of signaling cascades (like PI3K–Akt–mTOR) is observed; in myasthenia gravis, reduced MIRLET7C levels correlate with elevated IL‑10 expression; and in endometritis, overexpression of MIRLET7C can attenuate NF‑κB activation and downstream proinflammatory cytokine production. Moreover, MIRLET7C has been implicated in the modulation of the tumor microenvironment through its effects on macrophage polarization, microglial activation via TLR7 engagement, and mesenchymal stem cell function, thereby impacting both inflammatory cytokine production and angiogenesis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "23", "end_ref": "33"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its roles in oncogenesis and inflammation, MIRLET7C is a key regulator of stem cell differentiation and tissue homeostasis. Within mesenchymal stem cells from dental pulp and stem cells from the apical papilla, overexpression of MIRLET7C has been shown to inhibit osteo/odontogenic differentiation by repressing insulin-like growth factor receptor expression and modulating MAPK signaling cascades. Its function extends to the regulation of bone formation—in osteoporosis models, for example, where suppression of MIRLET7C enhances osteogenic activity by modulating SCD‑1 and activating Wnt/β‑catenin pathways—and to the control of cancer stem cell self-renewal, thereby increasing sensitivity to endocrine therapy in breast cancer. Furthermore, in ocular systems such as age-related cataract, MIRLET7C balances autophagy and apoptosis under oxidative stress conditions, underscoring its broader role in tissue regeneration and cellular stress responses."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "34", "end_ref": "38"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Dany Anglicheau, Vijay K Sharma, Ruchuang Ding, et al. 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