{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nTRIM59 is a member of the tripartite motif protein family that encodes a putative ubiquitin ligase and is emerging as a critical oncogenic driver in many human malignancies. Multiple studies have shown that TRIM59 is frequently upregulated in tumor samples from gastric cancer, non‐small cell lung cancer (NSCLC), colorectal carcinoma, osteosarcoma, breast cancer, cervical cancer, neuroblastoma, ovarian cancer, glioblastoma, hepatocellular carcinoma, and pancreatic and renal cancers. Elevation of TRIM59 correlates with enhanced proliferation, invasion, migration, and epithelial–mesenchymal transition, as well as with poorer patient prognoses and drug resistance. Its oncogenic properties have been linked to modulation of cell cycle regulators and anti‐apoptotic proteins, thereby promoting metastasis and tumor growth [."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "19"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nMechanistic studies reveal that TRIM59 mediates its diverse oncogenic effects through ubiquitin‐dependent modification of key substrates. It targets tumor suppressors such as p53, macroH2A1, and PPM1B, thereby modulating major signaling pathways including Ras, RB, STAT3, PI3K/AKT/mTOR, and ERK, as well as influencing NF‑κB and Wnt/β‑catenin cascades. In addition, TRIM59 regulates autophagy by modulating both the transcription and ubiquitination of BECN1 and influences the epithelial–mesenchymal transition by altering the balance of E‑cadherin, vimentin, and Snail expression. Such regulatory versatility positions TRIM59 as a nexus for the control of cellular proliferation, apoptosis, and metastasis [."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "20", "end_ref": "26"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its clear role in oncogenesis, TRIM59 functions in various non‐malignant pathologies and biological processes. Early cloning studies have highlighted its evolutionary conservation ["}, {"type": "fg", "children": [{"type": "fg_f", "ref": "27"}]}, {"type": "t", "text": "]. In addition to its involvement in tumorigenesis in esophageal, renal, and nasopharyngeal carcinomas ["}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "28", "end_ref": "30"}, {"type": "fg_f", "ref": "25"}]}, {"type": "t", "text": "], TRIM59 is also implicated in retinoblastoma ["}, {"type": "fg", "children": [{"type": "fg_f", "ref": "31"}]}, {"type": "t", "text": "], in the regulation of inflammatory responses in macrophages ["}, {"type": "fg", "children": [{"type": "fg_f", "ref": "32"}]}, {"type": "t", "text": "], and in endometriosis via activation of the transforming growth factor‐β/Smad pathway ["}, {"type": "fg", "children": [{"type": "fg_f", "ref": "23"}]}, {"type": "t", "text": "]. Furthermore, its modulation of innate immune signaling has been reported in osteoarthritis chondrocytes ["}, {"type": "fg", "children": [{"type": "fg_f", "ref": "24"}]}, {"type": "t", "text": "] and cerebral ischemia/reperfusion injury through ubiquitin‐mediated degradation of NLRP3 ["}, {"type": "fg", "children": [{"type": "fg_f", "ref": "33"}]}, {"type": "t", "text": "]. TRIM59 also drives neuroendocrine differentiation in prostate cancer ["}, {"type": "fg", "children": [{"type": "fg_f", "ref": "34"}]}, {"type": "t", "text": "] and is regulated by non‑coding RNAs in neuroblastoma ["}, {"type": "fg", "children": [{"type": "fg_f", "ref": "35"}]}, {"type": "t", "text": "]. Finally, its oncogenic activity extends to influencing cellular metabolism—as seen in ovarian cancer via effects on glycolysis—and contributing to drug resistance in lung adenocarcinoma and ferroptosis regulation in pancreatic cancer ["}, {"type": "fg", "children": [{"type": "fg_f", "ref": "36"}, {"type": "fg_f", "ref": "26"}, {"type": "fg_f", "ref": "34"}, {"type": "fg_f", "ref": "37"}]}, {"type": "t", "text": "].\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Zhicheng Zhou, Zhongzhong Ji, You Wang, et al. 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