{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nTRIM52 is emerging as an important oncogenic regulator whose overexpression drives tumorigenesis in several cancer types. For instance, in ovarian cancer, elevated TRIM52 expression enhances cell proliferation, invasion, and migration by activating the NF‑κB signaling cascade, while its knockdown induces apoptosis. In HBV‑associated hepatocellular carcinoma, TRIM52 levels are increased by the viral HBx protein, leading to enhanced cell proliferation through NF‑κB activation—even though its precise role in HCC remains under investigation. Moreover, in lung cancer, TRIM52 upregulation promotes cell cycle progression and invasiveness via stimulation of the Wnt/β‑catenin pathway. Complementing these findings, in diffuse large B cell lymphoma the long non‑coding RNA TRIM52‑AS1 functions to stabilize TRIM52 mRNA—by sequestering inhibitory microRNAs—thereby contributing to lymphoma progression."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "6"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its role in cancer, TRIM52 protein levels are exquisitely regulated. Although its mRNA is constitutively expressed, TRIM52 protein is extremely short‑lived—displaying one of the fastest turnover rates in the human proteome—due to rapid proteasomal degradation. Detailed structural analyses have shown that all of its domains, including an unexpected repetitive acidic loop within its expanded RING domain, contribute to its intrinsic instability, underscoring the tight control over this cell‑essential factor."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "7"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond oncogenesis, TRIM52 is also implicated in non‑neoplastic inflammatory disorders. In benign prostatic hyperplasia, it serves as a novel biomarker of prostate basal cells. Similarly, in temporomandibular joint osteoarthritis, TRIM52 is up‑regulated by interleukin‑1β, which, in turn, promotes cell proliferation, inflammatory responses, and oxidative stress through activation of the TLR4/NF‑κB pathway. These observations illustrate the multifaceted roles of TRIM52 in both tumorigenesis and inflammatory pathophysiology."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "8"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Wenchun Fan, Tingting Liu, Xiangmin Li, et al. 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"}, {"type": "b", "children": [{"type": "t", "text": "TRIM52 plays an oncogenic role in ovarian cancer associated with NF-kB pathway."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Cell Death Dis (2018)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1038/s41419-018-0881-6"}], "href": "https://doi.org/10.1038/s41419-018-0881-6"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "30185771"}], "href": "https://pubmed.ncbi.nlm.nih.gov/30185771"}]}, {"type": "r", "ref": 5, "children": [{"type": "t", "text": "Xiaoyan Mu, Hegen Li, Lei Zhou, et al. "}, {"type": "b", "children": [{"type": "t", "text": "TRIM52 regulates the proliferation and invasiveness of lung cancer cells via the Wnt/β‑catenin pathway."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Oncol Rep (2019)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.3892/or.2019.7110"}], "href": "https://doi.org/10.3892/or.2019.7110"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "31002351"}], "href": "https://pubmed.ncbi.nlm.nih.gov/31002351"}]}, {"type": "r", "ref": 6, "children": [{"type": "t", "text": "Fang Zhao, Shucheng Li, Jingjing Liu, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Long non-coding RNA TRIM52-AS1 sponges microRNA-577 to facilitate diffuse large B cell lymphoma progression via increasing TRIM52 expression."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Hum Cell (2022)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1007/s13577-022-00725-1"}], "href": "https://doi.org/10.1007/s13577-022-00725-1"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "35676608"}], "href": "https://pubmed.ncbi.nlm.nih.gov/35676608"}]}, {"type": "r", "ref": 7, "children": [{"type": "t", "text": "Kathrin Hacker, Stefan Benke, Benedikt Agerer, et al. "}, {"type": "b", "children": [{"type": "t", "text": "A repetitive acidic region contributes to the extremely rapid degradation of the cell-context essential protein TRIM52."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Sci Rep (2019)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1038/s41598-019-44359-0"}], "href": "https://doi.org/10.1038/s41598-019-44359-0"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "31133683"}], "href": "https://pubmed.ncbi.nlm.nih.gov/31133683"}]}, {"type": "r", "ref": 8, "children": [{"type": "t", "text": "Jianming Sun, Peng Liu, Jianmin Mao, et al. "}, {"type": "b", "children": [{"type": "t", "text": "TRIM52 positively mediates NF-κB to promote the growth of human benign prostatic hyperplasia cells through affecting TRAF2 ubiquitination."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Life Sci (2020)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1016/j.lfs.2020.118380"}], "href": "https://doi.org/10.1016/j.lfs.2020.118380"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "32898524"}], "href": "https://pubmed.ncbi.nlm.nih.gov/32898524"}]}, {"type": "r", "ref": 9, "children": [{"type": "t", "text": "Tie Ma, Chuan-Bin Wu, Qing-Xia Shen, et al. 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