{"id":237,"title":"An anti-invasion endogenous tRNA-derived small RNA (3'-tRFAlaAGC) alleviates endometriosis by suppressing MCCC1 mediated EMT","title_zh":"内源性抗侵袭 tRNA 衍生小 RNA（3'-tRFAlaAGC）通过抑制 MCCC1 介导的上皮-间质转化缓解子宫内膜异位症","url":"https://pubmed.ncbi.nlm.nih.gov/42982359","doi":"10.1016/j.cellsig.2026.112990","pmid":"42982359","journal":"Cell Signal","kind":"paper","lang":"en","published_at":"2026-11-04T00:00:00+00:00","fetched_at":"2026-11-08T03:44:00+00:00","authors":["Shi H","Zhang S","Hou H","Li T","He D","Jiang D","Cheng X","Ma L","Lin X","Liu Y","Ding Z","Ruan H","Fu Z","Shi X"],"primary_topic":"endometrium","topics":[{"slug":"endometrium","score":5.0,"hits":["endometrial","endometriosis"]},{"slug":"ai-compute","score":1.0,"hits":["machine learning"]}],"topic_score":5.0,"preference_score":0.0,"preference_labels":[],"llm_score":74.0,"final_score":82.0,"score_dims":{"novelty":82,"rigor":70,"impact":70,"relevance":72,"translation":73},"recommend_reason":"提出 tRNA 衍生小 RNA 通过 MCCC1-NF-κB-EMT 轴调控内异症侵袭的新机制，且兼具血清无创诊断（机器学习）与小鼠在体验证，对内异症机制与标志物研究有参考价值；但尚属动物与体外层面，临床转化证据有限。","keywords":["子宫内膜异位症","tRNA 衍生小 RNA","3'-tRFAlaAGC","MCCC1","上皮-间质转化","NF-κB"],"selected":1,"story_id":85,"llm_provider":"deepseek","llm_model":"deepseek-flash","llm_effort":"low","source_key":"pubmed-uterus-pregnancy","source_name":"PubMed · 内膜/植入/早孕","source_tier":1,"mention_count":1,"has_interpretation":false,"journal_key":null,"journal_tier":"cns-sub","journal_if":null,"is_mock":false,"summary_zh":"研究聚焦子宫内膜异位症的侵袭性机制，发现一种内源性 tRNA 衍生小片段 3'-tRFAlaAGC 在子宫内膜异位病灶及血清中下调，并可抑制异位内膜细胞的侵袭。机制上，3'-tRFAlaAGC 通过其独特结合位点（MCCC1 蛋白 383–494aa 区段）形成 3'-tRFAlaAGC-MCCC1 复合物，削弱 MCCC1 介导的 p65 核转位，从而抑制 NF-κB 通路激活及与疾病进展相关上皮-间质转化（EMT）。在子宫内膜异位症小鼠模型中，该片段可减轻病灶负荷；结合机器学习分析显示，血清中 3'-tRFAlaAGC 具有较好的预测效能。研究提示其作为诊断标志物与干预靶点的潜力，但队列规模与临床验证细节在摘要中未充分呈现。","summary":"Endometriosis is an invasive gynecological disorder, characterized by occult ectopic endometrial growth. Nascent endogenous tRNA-derived fragments occur across various disease, yet its pathology mechanistic pathways in endometriosis remain poorly defined. Downregulated 3'-tRFAlaAGC validated from endometrial lesions and serum was demonstrated to suppress the invasion of endometriosis. Indeed, we identified that nuclear translocation of p65 mediated by MCCC1 protein was attenuated due to the occurrence of 3'-tRFAlaAGC-MCCC1 compound relying on the 383-494aa of MCCC1, a unique binding site where 3'-tRFAlaAGC directly bond to MCCC1. Hence, the activation of NF-κB pathway was inhibited, hindering the epithelial-mesenchymal transition related to the progression of endometriosis. Moreover, 3'-tRFAlaAGC alleviated lesion burden in endometriosis mice, and the precious predictive efficiency in serum through the Machine learning. Understanding the 3'-tRFAlaAGC provides a critical opportunity to dissect the mechanisms driving endometriosis progression, opening new avenues to diagnose and halt endometriosis in its tracks.","interpretation_basis":null,"fulltext_status":null,"interpretation":null,"fulltext":{"available":false,"status":null,"reason":"尚未抓取全文（未入选、分数未达阈值，或还没跑 fulltext 步骤）","pmcid":null,"license":null,"chars":0,"source":null,"fetched_at":null}}