{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMIR511, notably expressed as miR‐511‑3p or miR‐511‑5p, plays important roles in the regulation of innate immune responses. In macrophages, miR‑511‑3p is co‐expressed with the mannose receptor (MRC1/CD206) and acts as an intrinsic “gatekeeper” by dampening protumoral genetic programs in tumor‐associated macrophages, thereby restraining tumor growth. In intestinal macrophages, modulation of miR‑511‑3p levels directly influences TLR4 mRNA abundance and thus controls inflammatory cytokine production in response to microbial stimuli. Moreover, in human monocytes, miR‑511‑5p mediates glucocorticoid and TGF‑β–induced endotoxin tolerance by targeting TLR4, thereby limiting excessive inflammation."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "3"}]}, {"type": "t", "text": "\n\nDis parturient studies have revealed diverse roles of MIR511 in tumor biology, where its function appears highly context dependent. In adenocarcinoma cells, miR‑511 (alongside miR‑1297) suppresses the oncogene TRIB2, leading to increased C/EBPα expression and reduced cell proliferation. In lung adenocarcinoma, enforced expression of miR‑511 restores radioresistance sensitivity by inducing G1‑S cell cycle arrest and boosting pro‐apoptotic BAX via TRIB2 downregulation. In hepatocellular carcinoma (HCC), divergent findings have been reported: one study indicates that increased miR‑511 levels promote cell proliferation through attenuation of the antiproliferative gene BTG1, whereas another demonstrates that miR‑511 downregulation enhances proliferation by upregulating PIK3R3 and activating the AKT/mTOR pathway. Similar tumor‐suppressive functions have been implicated in colorectal, gastric, osteosarcoma, retinoblastoma, and breast cancers, where miR‑511 (or its sponging by specific lncRNAs/circRNAs) modulates key effectors such as AKT3, PAK2, MAPK1, PAX6, and cell-cycle regulators including CCNE1 and CHEK1. These observations, derived from studies employing ceRNA network analyses and functional assays, suggest that MIR511 can act as a tumor suppressor in many contexts, although its activity may vary with cellular environment and regulatory network composition."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "4", "end_ref": "16"}]}, {"type": "t", "text": "\n\nAliquet etiam, MIR511 has been implicated in diverse non‐oncogenic pathological processes. In children with combined pituitary hormone deficiency, elevated serum miR‑511 levels correlate with reduced PROP1 expression, offering promise as a non‑invasive biomarker. In the nervous system, miR‑511 regulates FKBP5 thereby modulating neuronal differentiation, with implications for neuropsychiatric disorders; related inflammation‐linked functions may also play a role in Alzheimer’s disease. Furthermore, in allergic rhinitis, exosomal lncRNA (NEAT1) sequesters miR‑511, leading to dysregulation of NR4A2 and contributing to inflammation and mucus production."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "17", "end_ref": "20"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Mario Leonardo Squadrito, Ferdinando Pucci, Laura Magri, et al. 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