{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nUBE2T functions as a critical E2 ubiquitin‐conjugating enzyme in the Fanconi anemia (FA) DNA repair pathway, where it cooperates with the E3 ligase subunit FANCL to monoubiquitinate FANCD2 and FANCI in response to DNA‐interstrand crosslinks. This post‐translational modification is essential for proper DNA damage repair, with studies demonstrating that a deficiency or mutation in UBE2T leads to chromosomal abnormalities typical of FA. In addition, UBE2T undergoes auto‐monoubiquitination that appears to serve as a built‐in negative regulatory mechanism, and in some cases, spontaneous genetic reversion events have been observed in FA patients, underscoring its central role in maintaining genomic integrity."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "9"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its canonical role in DNA repair, aberrant overexpression of UBE2T has been implicated in the oncogenic progression of a wide spectrum of human cancers. Elevated UBE2T levels have been reported in lung, breast, prostate, nasopharyngeal, gastric, hepatocellular, multiple myeloma, cholangiocarcinoma, esophageal, clear cell renal cell, and ovarian carcinomas, among others. In these contexts, UBE2T drives malignant behaviors by promoting cell proliferation, migration, invasion and epithelial–mesenchymal transition (EMT), while also conferring resistance to radiotherapy and chemotherapy. Mechanistically, UBE2T facilitates the ubiquitination and consequent degradation of pivotal tumor suppressors (such as p53 and FOXO1) and modulates key oncogenic signaling pathways including Wnt/β‐catenin, PI3K/Akt/mTOR, and ERK/MAPK. The cumulative effect of these processes is a more aggressive tumor phenotype that correlates with higher pathological grade, advanced stage, and poorer patient prognosis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "10", "end_ref": "30"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAt the mechanistic level, UBE2T regulates tumor cell behavior through the ubiquitination of diverse substrates and is itself subject to multiple layers of regulation. Transcriptional upregulation by factors such as E2F5 and post‐transcriptional control by microRNAs—including miR-543 in breast cancer and miR-498 in malignant melanoma—further influence its oncogenic functions. UBE2T also modulates cancer stem cell properties via interactions with proteins such as the E3 ubiquitin ligase Mule, and its enzymatic activity has been exploited to identify a novel allosteric pocket amenable to small-molecule inhibition. Comprehensive pan-cancer analyses and reviews further underscore the multifaceted role of UBE2T in tumorigenesis and therapeutic resistance, highlighting its potential as both a prognostic biomarker and a promising target for drug development."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "31", "end_ref": "38"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Yuichi J Machida, Yuka Machida, Yuefeng Chen, et al. 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