{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMiR-326 has emerged as a key regulator of immune function and fibrosis. In autoimmune conditions such as multiple sclerosis, miR-326 promotes the differentiation of Th17 cells by directly targeting negative regulators like Ets‑1, with its expression closely correlating with disease severity. In addition, alterations in miR-326 levels have been implicated in other immune‐mediated states, including type 1 diabetes, as well as in fibrotic processes in pulmonary and endometrial tissues via modulation of TGF‑β1/Smad3 signaling."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "5"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn the context of cancer, miR-326 predominantly functions as a tumor suppressor and prognostic biomarker across a broad spectrum of malignancies. In gliomas, for instance, overexpression of miR-326 triggers apoptosis, cell cycle arrest, and reduced metabolic activity by targeting oncogenes and components of the Notch and Hedgehog pathways. Similar anti‐tumor effects have been documented in non‑small cell lung cancer, colorectal cancer, pancreatic ductal adenocarcinoma, endometrial, and gastric cancers, where miR-326 suppresses proliferation, migration, and invasion by downregulating key factors such as CCND1, NOB1, FSCN1, and NSBP1. Moreover, its diminished expression has been linked to aggressive disease phenotypes and poorer clinical outcomes in osteosarcoma and other tumors."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "6", "end_ref": "17"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its direct tumor‐suppressive activities, miR-326 modulates chemoresistance and intricate intracellular signaling through competitive endogenous RNA (ceRNA) networks. Downregulation of miR-326 is associated with multidrug resistance by influencing drug efflux transporters such as MRP1 and through interactions with ABCB1 transcripts. In several cancers, long noncoding RNAs and circular RNAs—including SNHG1, HOTAIR, PCAT1, and specific circRNAs—act as molecular sponges to sequester miR-326, thereby derepressing targets involved in proliferation, invasion, and survival (for example, SP1, FUT6, CCL5, and components of the Wnt/β‑catenin pathway). Such ceRNA interactions have been documented not only in solid tumors like esophageal and rectal cancers but also in leukemia, where reduced miR-326 correlates with chemoresistance. Additionally, emerging roles in other contexts, such as regulation of proteases (e.g., ADAM17) in lung adenocarcinoma, modulation of Hedgehog signaling in medulloblastoma, and control of apoptosis in platelets via Bcl‑xL targeting, further underscore the multifaceted biological functions of this microRNA."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "18", "end_ref": "26"}, {"type": "fg_f", "ref": "19"}, {"type": "fg_f", "ref": "21"}, {"type": "fg_fs", "start_ref": "27", "end_ref": "39"}, {"type": "fg_f", "ref": "13"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Changsheng Du, Chang Liu, Jiuhong Kang, et al. 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