Page 26 - 南京医科大学自然版

南京医科大学学报（自然科学版） 第44卷第6期
·762 · Journal of Nanjing Medical University（Natural Sciences） 2024年6月

·基础研究·

UBE2T通过JAK⁃STAT通路促进甲状腺乳头状癌细胞增殖

张丽君，李 琳，斯 岩，沈美萍 *
南京医科大学第一附属医院普外科，江苏 南京 210029

［摘 要］ 目的：探讨泛素结合酶 E2T（ubiquitin⁃binding enzyme E2T，UBE2T）在人甲状腺乳头状癌（papillary thyroid carcino⁃
ma，PTC）中的表达情况及其对患者预后的影响，同时探讨UBE2T在PTC细胞中的功能，旨在识别其可能的调控机制，为未来
PTC的靶向治疗策略提供理论依据。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 Western blot 技术检测 UBE2T 在甲状腺肿瘤组织和癌旁正常组织中的表达。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、划痕和Transwell实验评估细胞增殖、迁移和侵袭
能力，并通过Western blot检测相关蛋白水平的变化。结果：TCGA数据库生物信息学分析表明，PTC组织中UBE2T显著升高，
且其表达与患者无疾病间隔、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
细胞迁移和侵袭，诱导STAT磷酸化下调。敲减UBE2T的细胞系加入STAT激活剂后，细胞增殖显著提高。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。
［关键词］ 甲状腺乳头状癌；泛素结合酶 E2T；JAK⁃STAT 通路
［中图分类号］ R736.1 ［文献标志码］ A ［文章编号］ 1007⁃4368（2024）06⁃762⁃07
doi：10.7655/NYDXBNSN240139

UBE2T enhances the proliferation of papillary thyroid carcinoma cells through the JAK⁃
STAT pathway

*
ZHANG Lijun，LI Lin，SI Yan，SHEN Meiping
Department of General Surgery，the First Affiliated Hospital of Nanjing Medical University，Nanjing 210029，China

［Abstract］ Objective：This study aims to investigate the expression of ubiquitin⁃binding enzyme E2T（UBE2T）in papillary thyroid
carcinoma（PTC）tissues and its effect on patient prognoses. Additionally，the effects of UBE2T on PTC cell function were explored，

aiming to identify potential regulatory pathways and provide theoretical foundations for future targeted therapies. Methods：By using
The Cancer Genome Atlas（TCGA）database，the UBE2T expression in PTC tissues and its association with patient prognosis were
systematically analyzed. The UBE2T expression in tumor tissues and adjacent normal tissues of thyroid were assessed by Western blot.
UBE2T knockdown experiments were performed in PTC cell lines（TPC⁃1 and KTC⁃1）. Cell proliferation，migration，and invasion
abilities were evaluated by using CCK⁃8 and colony formation，wound healing and Transwell assays，respectively，with Western blot
measuring protein levels. Results：The TCGA analysis revealed significantly elevated UBE2T expression levels in PTC tissues，
correlated with disease⁃free interval and lymph node metastasis（P < 0.01）. The UBE2T knockdown led to decreased proliferation，
migration，and invasion ability in TPC⁃1 and KTC⁃1 cells，accompanied by the reduced STAT phosphorylation levels. The proliferation
of UBE2T ⁃ knockdown cells significantly increased when treated with a STAT activator. Conclusion：The UBE2T knockdown
suppresses the proliferation，migration，and invasion of PTC cell lines，suggesting UBE2T as a potential therapeutic target for PTC by
modulating the JAK⁃STAT signaling pathway.
［Key words］ papillary thyroid carcinoma；ubiquitin⁃binding enzyme E2T；JAK/STAT pathway
［J Nanjing Med Univ，2024，44（06）：762⁃768］

［基金项目］ 江苏省科教能力提升工程（江苏省医学重点学科ZDXK202222）
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通信作者（Corresponding author），E⁃mail：shenmeiping@jsph.org.cn