{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMiR‑1294 is a microRNA that in many studies has emerged as a tumor suppressor, with its reduced activity contributing to oncogenesis in a spectrum of cancers. In pancreatic ductal adenocarcinoma, esophageal squamous cell carcinoma, osteosarcoma, gastric cancer, hepatocellular carcinoma, epithelial ovarian cancer, and glioma, decreased miR‑1294 function has been observed to promote cell proliferation, invasion, metastasis, and chemoresistance. In these settings, oncogenic circular RNAs—including circ_0030235, circLDLR, circ_0004370, circ‑PRKCI, circUBAP2, circ_0005198, circ_0000936, and circ_0023984—act as molecular sponges to sequester miR‑1294, thereby relieving repression of downstream targets such as LASP1, FOXK1, CYP19A1, c‑Myc, TEAD1/PIM1, and HMGA1. Notably, in polycystic ovary syndrome, reduced levels of exosomal circ_0006877 allow miR‑1294 to modulate key genes in estrogen biosynthesis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "13"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its role in oncogenesis, miR‑1294 also contributes to immune regulation and inflammatory signaling. For example, miR‑1294 has been shown to activate endosomal Toll‑like receptor 8, leading to NF‑κB activation and the consequent induction of pro‑inflammatory cytokines such as IL‑8, IL‑1β, and TNF‑α—a mechanism that may contribute to autoimmune disorders. In parallel, studies in atopic dermatitis models have identified STAT3 as a direct target of miR‑1294; upregulation of miR‑1294 in these systems alleviates inflammatory responses and helps preserve epidermal barrier integrity, thereby highlighting its potential as a therapeutic target in inflammatory skin conditions."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "14"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Yi Xu, Yue Yao, Ping Gao, et al. 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