江苏省人民医院南京医科大学第一附属医院普外科
Department of General Surgery, The First Affiliated Hospital with Nanjing Medical University
目的：本研究旨在深入探讨泛素结合酶E2T（Ubiquitin-Binding Enzyme E2T，UBE2T）在人甲状腺乳头状癌（Papillary Thyroid Carcinoma，PTC）中的表达情况及其对患者预后的影响，同时探讨UBE2T对PTC细胞生物学行为的直接影响，旨在识别其可能的调控通路，为未来治疗PTC的靶向策略提供理论依据。方法：采用癌症基因组图谱（The Cancer Genome Atlas，TCGA）数据库，系统分析UBE2T在PTC中的表达及其与患者预后的关系。通过蛋白印迹（Western Blotting , WB）技术检测UBE2T在甲状腺正常和肿瘤组织中的表达。在PTC细胞系（TPC-1、KTC-1）中进行UBE2T敲减实验，借助CCK-8、平板克隆、Transwell和划痕实验评估细胞增殖、迁移和侵袭能力，并通过WB检测相关蛋白水平的变化。结果：TCGA数据库生物信息分析表明，PTC组织中UBE2T显著升高，且其表达与患者无疾病间隔（Disease-free Interval , DFI）、淋巴结转移相关（P <0.01）。UBE2T敲减导致TPC-1和KTC-1细胞增殖活力显著下降，同时抑制侵袭和迁移，诱导STAT磷酸化下调。敲减UBE2T的细胞系加入STAT激活剂后，细胞增殖显著升高，侵袭和迁移无显著差异结论：敲减UBE2T能抑制PTC细胞系TPC-1和KTC-1的增殖、迁移和侵袭，UBE2T通过调控JAK-STAT信号通路促进细胞增殖，提示UBE2T有可能成为PTC的治疗靶点。
Objective: This study aims to investigate the expression of Ubiquitin-Binding Enzyme E2T (UBE2T) in Papillary Thyroid Carcinoma (PTC) and its impact on patient prognosis. Additionally, we explore UBE2T's direct effects on PTC cell biology, aiming to identify potential regulatory pathways and provide theoretical foundations for future targeted therapies. Methods: Utilizing The Cancer Genome Atlas (TCGA) database, we systematically analyzed UBE2T expression in PTC and its correlation with patient prognosis. Western blotting (WB) assessed UBE2T expression in thyroid normal and tumor tissues. UBE2T knockdown experiments were conducted in PTC cell lines (TPC-1, KTC-1) using CCK-8, colony formation, Transwell, and scratch assays to evaluate proliferation, migration, and invasion abilities, with WB measuring protein level changes.Results: TCGA analysis revealed significantly elevated UBE2T in PTC tissues, correlating with disease-free interval and lymph node metastasis (P <0.01). UBE2T knockdown led to decreased proliferation, inhibited invasion and migration in TPC-1 and KTC-1 cells, accompanied by reduced STAT phosphorylation. Adding a STAT activator in UBE2T-knockdown cells significantly increased proliferation without significant changes in invasion and migration. Conclusion: UBE2T knockdown suppresses proliferation, migration, and invasion in PTC cell lines, suggesting UBE2T as a potential therapeutic target for PTC by modulating the JAK-STAT signaling pathway.
