{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nTRIM14 functions as a key mitochondrial adaptor in the innate antiviral immune response. Localized on the outer mitochondrial membrane, it interacts with MAVS and facilitates the assembly of the signaling complex that activates RIG-I–dependent pathways, leading to type I interferon and NF‐κB pathway activation. Post‐translational modifications, including Lys-63-linked ubiquitination and regulation through its PRYSPRY domain, are critical for its ability to recruit downstream modulators. Moreover, TRIM14 expression is itself induced as an interferon-stimulated gene via IRF1 and STAT1, and its antiviral actions include targeting and promoting the degradation of viral proteins, thereby restricting infections by hepatitis C virus, influenza A virus, and alphaviruses."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "8"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its antiviral role, TRIM14 is frequently deregulated in various cancers, where it primarily acts as an oncogene. Elevated TRIM14 levels have been reported in oral, osteosarcoma, glioma, tongue squamous, gastric, breast, papillary thyroid, melanoma, hepatocellular, and acute myeloid leukemia tumors. Overexpression in these malignancies correlates with enhanced cell proliferation, epithelial–mesenchymal transition, invasiveness, metastasis, and resistance to chemotherapy. Mechanistically, TRIM14 promotes oncogenic signaling through activation of pathways such as AKT, STAT3, canonical Wnt, and NF‐κB, while its own expression is modulated by several microRNAs (including miR-195-5p, miR-15b, miR-4443, miR-1296-5p, and miR-671-5p). Therapeutic strategies targeting TRIM14, such as bispecific antibodies, have shown promise in preclinical models."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "9", "end_ref": "23"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nConversely, in certain contexts such as non-small-cell lung carcinoma (NSCLC), TRIM14 appears to have tumor-suppressive properties. Here, reduced TRIM14 expression is associated with increased tumor growth, decreased apoptotic responsiveness, and impaired interferon-STAT1 signaling. In these cells, TRIM14 contributes to the degradation of key metabolic enzymes via ubiquitination, underscoring its context-dependent functions in cancer biology."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "24"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its roles in immunity and oncogenesis, TRIM14 has also been implicated in modulating inflammatory processes. In osteoarthritis, increased TRIM14 expression correlates with chronic inflammatory pain by promoting the degradation of IκBα and consequent activation of NF-κB signaling, suggesting that TRIM14 may represent a novel target for managing inflammatory pain."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "26"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Zhuo Zhou, Xue Jia, Qinghua Xue, et al. 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